cell proliferation

This research examined the connection between circulating FGF21 and clinicopathological findings in papillary thyroid carcinoma.

This analytical cross-sectional research was conducted on patients with papillary thyroid cancer at the Seyyed Shirazi Endocrinology Clinic in Gorgan, Iran. Laboratory data, including demographics, ultrasonography and pathology reports, and FGF21 levels, were collected. The data was analyzed with SPSS 25. Normal distribution was evaluated by using Kolmogorov-Smirnov and Shapiro-Wilk tests. Group differences were evaluated with Chi-square, independent sample t-test and Mann-Whitney U tests. A p-value less than 0.05 was considered significant.

In this research, 83% of patients were female, and the mean±SD age was 42.51±13.28 years old. The mean±SD and FGF21 concentrations in 49 patients were 716.41±458.7, the median was 489 pg/ml, and 24 (49%) patients were in the high FGF21 group. There was no statistically significant relation between FGF21 level and age (P=0.95), sex (P=>0.99), tumor size (P=0.68), tumor stage (P=>0.99), lymphadenopathy (P=>0.99), lymph node metastasis (P=0.24), triglycerides (P=0.93), total cholesterol (P=0.47), LDL (P=0.08), and HDL (P=0.08). However, FGF21 levels were significantly associated with fasting blood glucose (P=0.03), body mass index (BMI) (P=<0.0001), capsular invasion (P=0.001), lymphovascular involvement (P=0.0001) and Thyroid Imaging Reporting and Data System (TIRADS) score (P=0.02). In addition, high levels of FGF21 were found to be 78.95% sensitive and 70% specific for capsular invasion.

Our study demonstrated that FGF21 is associated with more severe papillary thyroid cancer clinicopathological features such as capsular invasion, lymphovascular involvement, TIRADS score, and BMI.

One of the leading causes of endometriosis is the return of menstrual blood flow into the pelvic cavity and the establishment of menstrual blood mesenchymal stem cells (MenSCs) outside the uterus. MenSCs from endometriosis patients (E-MenSCs) and healthy women have been shown to vary in terms of surface markers and gene expression, which may suggest the involvement of these cells in the development and expansion of ectopic lesions. This study aimed to investigate the effects of beta-catenin signaling inhibitor C-82 and naringenin as PI3K signaling pathway inhibitors on E-MenSCs to modulate their gene expression and functional pattern. 

Briefly, E-MenSCs isolated by density-gradient centrifugation were treated with C-82 and naringenin, and the genes and pathways related to inflammation, proliferation, and survival were evaluated. E-MenSCs showed increased early apoptosis and decreased levels of ROS, IL-6 and IL-8, ER, α-SMA, and Ki-67 protein expression. 

Our results shed light on the function of C-82 and naringenin in modulating E-MenSCs. 

However, more research is needed to analyze the precise effects of small molecule C-82 and naringenin on endometriosis.

LOXL2, known as Lysyl oxidase-like 2, is classified as a lysyl oxidase (LOX) family member. However, its role and mechanism in endometrial cancer (EC) are unknown. Therefore, we aimed to investigate the potential role and mechanism of LOXL2 in EC.

The levels of LOXL2 expression in EC tissues and normal adjacent tissues were evaluated by immunohistochemically (IHC) labeling. Following the dye application, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Transwell methodologies were executed to evaluate the effects of LOXL2 inhibition and up-regulation on the growth, programmed cell death, migration, and susceptibility to iron-dependent cell death of EC. Moreover, protein analysis through Western blotting and gene expression analysis using Real-time quantitative PCR (RT-qPCR) was employed to measure the levels of pertinent biomarkers.

LOXL2 is highly expressed in both EC tissues and serum in vivo. Silencing LOXL2 reduced EC cell proliferation and migration while increasing apoptosis in vitro. LOXL2 silencing increased the ferroptosis-related proteins Solute Carrier Family 7 Member 11 (SLC7A11) and Ferritin Heavy Chain 1 (FTH1) while decreasing Glutathione Peroxidase 4 (GPX4) (both, P<0.001). Additionally, LOXL2 silencing reduced the p-PI3K and p-Akt protein expression, while LOXL2 overexpression (OE-LOXL2) elevated the p-PI3K and p-Akt protein expression (both, P<0.001). Additionally, LOXL2 silencing increases SLC7A11 and FTH1 while decreasing GPX4 (both P<0.001). LOXL2 overexpression has the opposite effect. However, the LY294002 inhibitor restores SLC7A11 and FTH1 expression while decreasing GPX4 (P<0.001).

Our research demonstrated that LOXL2 might protect EC via phosphorylation by activating the PI3K/AKT pathway.

Ferula gummosa Boiss. is a widely recognized species native to Iran, primarily found in the northern and northeastern regions. It has long been valued for its medicinal properties, particularly in traditional medicine, where its gum is used to treat various gastrointestinal disorders and infections.

However, despite its established benefits, there is a significant research gap regarding its potential anti-cancer properties, specifically against skin cancer cells.

This study aimed to assess the cytotoxic and inhibitory effects of the gum of F. gummosa on the A-375 cell line using several assays, including MTT, clonogenic, acridine orange/ethidium bromide (AO/EtBr) staining, DNA degradation, and in vitro wound-healing experiments.

The findings revealed that the gum exhibited notable cytotoxicity on A-375 cells, achieving a 50% inhibitory concentration (IC 50 ) at 8 µg/mL after 48 hours of treatment (compared to control cells) (P < 0.01). The observed DNA degradation pattern suggested a reduction in cell viability, likely due to apoptosis induction. Microscopic examinations showed nuclear condensation and a significant suppression of colony formation in A-375 cells treated with 8 and 10 μg/mL concentrations of the gum, compared to untreated cells. Additionally, wound-healing assessments demonstrated the gum’s ability to inhibit cell migration in contrast to the untreated group.

These findings suggest that F. gummosa exhibits significant inhibitory effects on melanoma cancer cells, making it a promising candidate for further investigation.

Pancreatic ductal adenocarcinoma (PDAC) is a common digestive system tumor with high mortality rates and a poor prognosis. Reports suggest that microRNA (miR)-486-3p in PDAC can be used as a diagnostic biomarker. This research aimed to elucidate the mechanisms by which miR-486-3p regulates PDAC progression. miR-486-3p and chymotrypsin C (CTRC) expression in PDAC were measured using quantitative real-time polymerase chain reaction. Changes in the biological properties of PDAC cells were assessed by Transwell assay, scratch-wound assay, cell counting kit (CCK)-8 assay, and plate cloning assay. The protein expression of immunosuppressive factors (vascular endothelial growth factor, interleukin-6, and transforming growth factor-β) in PDAC cells was detected by western blot. Additionally, a subcutaneous graft tumor model was constructed to explore the influence of silencing miR-486-3p on PDAC in vivo. PDAC showed a pronounced increase in miR-486-3p expression. Upregulation of miR-486-3p stimulated PDAC cell proliferation, migration, invasion, and immunosuppressive factor protein expression, whereas silencing miR-486-3p hindered PDAC malignant development. miR-486-3p targets and negatively regulates CTRC expression. Silencing CTRC partially rescued the restraining impact of silencing miR-486-3p on PDAC malignant progression. In vivo experiments also indicated that silencing miR-486-3p inhibited PDAC malignant progression and immunosuppressive factor expression in vivo. In summary, miR-486-3p promotes immunosuppressive factor protein expression by targeting and negatively regulating CTRC expression, which in turn promotes PDAC malignant progression.

 The adhesion ability of mesenchymal stem cells can significantly affect their viability and is considered a prerequisite for cell therapy. The current study sought to evaluate the effect of fibroblast growth factor 2 (FGF2) and low-level laser therapy (LLLT), either individually or in conjunction, on the adhesion and proliferation of periodontal ligament stem cells (PDLSCs) when applied on the first day of cell seeding.

 The experimental groups of this study comprised a control group and different combinations of adjunctive FGF2 (50 ng/mL) and LLLT with an 808 nm diode laser in one (LLLT1) or two sessions (LLLT-2) of irradiation. The proliferation and adhesion of cells were evaluated by using the methylthiazolyl tetrazolium (MTT) assay and 4′,6-diamidino-2-phenylindole (DAPI) staining. All experiments were done in triplicates on the first, third, and fifth days after cell seeding. Two-way ANOVA and post hoc Tukey tests were used to analyze the data of the MTT assay. P<0.05 was considered statistically significant.

 One-day post-culture, only significant differences were found between the control group and the FGF2 (P=0.04) and FGF2+LLLT-2 application (P=0.04) groups. After three days post-cell culture, only a significantly higher proliferation rate was found in the control group than in the FGF2 group (P=0.01). After five days, the control group and LLLT-2 groups showed significantly higher amounts of proliferation compared to the other groups (P<0.05). DAPI staining qualitatively confirmed the results of the MTT assay.

 The LLLT can be applied to PDLSCs on the day of seeding without causing a notable decrease in their viability and adhesion. Conversely, the administration of FGF2 should be restricted on the seeding day and postponed to subsequent days as it may have adverse effects on their adhesion and proliferation.

This study investigated the inhibitory effect of apatinib on lung cancer cells with high expression of vascular endothelial growth factor-2 (VEGFR-2) and on inducing cellular autophagy and drug resistance. 

The expression of VEGFR-2 was detected using western blotting and RT-PCR. Cell proliferation was measured using the CCK8 and colony formation assays. The cell apoptosis rate was determined using flow cytometry and tunnel assay. Cellular autophagy was detected by measuring the expression of LC3-II using Western blotting and cellular immunofluorescence. The inhibitory effect of apatinib on lung cancer cells and transplanted tumors was observed after treatment with the autophagy inhibitor chloroquine. 

Apatinib dose-dependently inhibited the proliferation of H1975 and H446 cells; it induced apoptosis via the PARP and caspase 3 pathways in H1975 and H446 cells and effectively inhibited the growth of transplanted tumors. Apatinib induced autophagy in a dose-dependent manner in H1975 and H446 cells. The inhibitory effect of apatinib on cells and the promotion of apoptosis were significantly enhanced after treatment with chloroquine. Immunohistochemistry showed that combining apatinib with chloroquine could reduce the expression of CD31 and Ki67 and increase the expression of caspase 3. 

Apatinib inhibits proliferation and induces apoptosis in H1975 and H1446 lung cancer cells with high VEGFR2 expression and autophagy in H1975 and H446 cells.

 This manuscript explores the potential of dual glucagon-like peptide 1 (GLP-1) agonists combined with degludec basal insulin as a treatment approach for early type 1 diabetes. The study aims to evaluate the efficacy and mechanistic impact of semaglutide, a GLP-1 agonist, on newly diagnosed type 1 diabetes patients.

 A retrospective analysis was conducted to assess the effects of semaglutide on individuals with early type 1 diabetes. The analysis focused on the elimination of prandial and basal insulin, changes in C-peptide levels, and overall glycemic control. The study also examined the potential for GLP-1 agonists to protect residual beta cells, stimulate cell proliferation, and reprogram liver cells into insulin-producing cells. Additionally, the modification of GLP-1 agonists with albumin ligands to extend their half-life and enhance their anti-diabetic effects was investigated.

 The findings demonstrate the elimination of both prandial and basal insulin requirements, an increase in C-peptide levels, and improved glycemic control among the patients. Despite the positive outcomes, the study’s retrospective nature and absence of a control group highlight the necessity for larger, prospective trials.

 GLP-1 agonists show considerable potential in the management of type 1 diabetes by protecting residual beta cells, promoting cell proliferation, and reprogramming hepatic cells. The integration of modified GLP-1 agonists with albumin ligands could further enhance these effects. The manuscript underscores the need for continued research to fully explore this therapeutic approach. The proposed treatment strategy, which combines the autoimmune hypothesis, the proliferative effects of GLP-1, and albumin ligand modifications, aims to restore beta cell mass and function, thereby improving the quality of life for individuals with type 1 diabetes. Clinical trials are planned for 2024 under the registration ‹Amr Ahmed, Maher M. Akl, Semaglutide GLP1 Agonists with Degludec Basal-bolus Insulin in Early Type 1 Diabetes to Basalbolus› (ClinicalTrials.gov Identifier NCT06057077).

Enhancement of proliferation, pluripotency, and self-renewal capacity as the unique features of MSCs can improve their therapeutic potential to regenerate tissues. In this context, crocin and curcumin, carotenoid compounds with outstanding medicinal properties, could be promising for cell protection and growth. This study aimed to evaluate the impact of nanocurcumin and crocin on BM-MSCs proliferation and pluripotency in vitro.

BM-MSC were isolated from the iliac crest of SCI patients who were candidates for stem cell therapy. The effect of crocin and nanocurcumin on MSC proliferation was evaluated using MTT and PDT assay. The percentage of apoptotic MSCs was measured by flow cytometry. Furthermore, mRNA and protein expression of OCT4 and SOX2 as the proliferation and self-renewal related genes were quantified by real-time PCR and western blotting, respectively.

Our findings demonstrated that only low concentrations of nanocurcumin (0.3 and 0.7  µM) and crocin (2.5 5 µM) significantly affected MSCs proliferation and protected them from apoptosis. Also, crocin and nanocurcumin at low doses caused an elevation in the mRNA and protein expression levels of OCT4 and SOX2 genes. In contrast, high concentrations decreased the survival of MSCs and led to increased apoptosis compared with the untreated group.

Our results suggest that using nanocurcumin and crocin separately in culturing MSCs can be considered proliferative agents to prepare the more advantageous tool for cell therapies. However, more in vitro and preclinical research is needed in this area.

Although exogenous nitric oxide (NO) is used as medicine, in the previous we showed its inhibitory effect on the proliferation ability of rat bone marrow mesenchymal stem cells (BMSCs). In the present investigation, the inhibitory role of exogenous NO on BMSCs cell cycle was studied.

BMSCs after the third passage were treated for one hour every 48 hours with 100μM of sodium nitroprusside as an NO donor. Then, after 5,10,15, and 20 days of treatment, the viability, proliferation, and cell cycle of the BMSCs was investigated. In addition, the expression of the Raf1, CDK2, CDK4, P53, and GAPDH genes was studied.

Cell treatment caused a significant reduction in viability and proliferation at 5,10,15, and 20 days. Also, the treatment caused cell cycle arrest at G1 after 20 days. In addition, it was found that the CDK2 and CDK4 expression were down-regulated whereas the P53 expression was up-regulated, but the expression of Raf1 as well as GAPDH remained the same.

This study showed that prolonged treatment with a NO donor arrest the BMSCs cell cycle due to overexpression of P53, which inhibits the expression of Cdk2 and Cdk4.

An optimal culture medium that can rapidly and efficiently proliferate cells ex vivo is very crucial for developing mesenchymal stem cells (MSCs)-based tissue engineering and regenerative medicine. We developed a set of MSCs ex vivo proliferation medium, mscGOTM XF, which consists of a basal medium and a screened human platelet lysate. In this study, the developed mscGOTM XF medium was prepared, and then testified by human MSCs isolated from bone marrow, umbilical cord, and fat tissue. The proliferation, surface markers, differentiation, and chromosomal stability of MSCs cultured in mscGOTM XF medium were investigated. The mscGOTM XF medium could sustain MSCs at a high proliferation rate, with the population doubling time of 16 to 39 hours (depending on the type and passage number of MSCs). The proliferated MSCs could express CD105, CD90, and CD73, lack expression of CD34 and CD45; and maintain the capacity to differentiate into adipocytes, osteoblasts, and chondrocytes. Additionally, G-Band karyotyping data confirmed chromosome stability in the duration of cell culture at passage 5 and passage 7. The mscGOTM XF medium could sustain MSCs proliferation ex vivo and exhibit the potential to be developed into a clinical-grade cell culture medium kit.

 The endothelial cells derived from the human vein cord (HUVECs) are used as in-vitro models for studying cellular and molecular pathophysiology, drug and hormones transport mechanisms, or pathways. In these studies, the proliferation and quantity of cells are important features that should be monitored and assessed regularly. So rapid, easy, noninvasive, and inexpensive methods are favorable for this purpose.

 In this work, a novel method based on fast Fourier transform square-wave voltammetry (FFTSWV) combined with a 3D printed electrochemical cell including two inserted platinum electrodes was developed for non-invasive and probeless rapid in-vitro monitoring and quantification of human umbilical vein endothelial cells (HUVECs). The electrochemical cell configuration, along with inverted microscope images, provided the capability of easy use, online in-vitro monitoring, and quantification of the cells during proliferation.

 HUVECs were cultured and proliferated at defined experimental conditions, and standard cell counts in the initial range of 12 500 to 175 000 were prepared and calibrated by using a hemocytometer (Neubauer chamber) counting for electrochemical measurements. The optimum condition, for FFTSWV at a frequency of 100 Hz and 5 mV amplitude, were found to be a safe electrochemical measurement in the cell culture medium. In each run, the impedance or admittance measurement was measured in a 5 seconds time window. The total measurements were fulfilled at 5, 24, and 48 hours after the seeding of the cells, respectively. The recorded microscopic images before every electrochemical assay showed the conformity of morphology and objective counts of cells in every plate well. The proposed electrochemical method showed dynamic linearity in the range of 12 500-265 000 HUVECs 48 hours after the seeding of cells.

 The proposed electrochemical method can be used as a simple, fast, and noninvasive technique for tracing and monitoring of HUVECs population in in-vitro studies. This method is highly cheap in comparison with other traditional tools. The introduced configuration has the versatility to develop electrodes for the study of various cells and the application of other electrochemical designations.

Programmed death ligand‑1 (PD‑L1) is a pivotal inhibitory checkpoint ligand known to induce T-cell exhaustion via interaction with the programmed death‑1 (PD‑1) receptor. Beyond this, PD-L1’s intrinsic signaling pathways within cancer cells warrant further exploration. This study aims to elucidate the effect of PD-L1 stimulation on the proliferation, survival, and apoptosis of acute myeloid leukemia (AML) cell lines. Two human AML cell lines, HL-60 and THP-1 were cultured and treated with phorbol 12-myristate 13-acetate (PMA) to induce PD-L1overexpression. Post-treatment PD-L1 expression was confirmed via flow cytometry. Subsequently, cell surface PD-L1 was stimulated using a recombinant PD-1, 24 hours post-PMA treatment. The expression alterations in pivotal genes including BCL2, MKI67, BAX, and CASP3 were monitored using quantitative real-time polymerase chain reaction 24 and 48 hours post-treatment. Additionally, annexin-V through flow cytometry. Findings reveal that PD-L1 stimulation augments AML cell proliferation and survival by enhancing MKI67 and BCL2 expressions while concurrently inhibiting cell apoptosis due to decreased BAX and CASP3 expression following PD-L1 stimulation. Notably, stimulated cells expressed exhibited reduced annexin-V compared to control cells. This study underscores that PD-L1 stimulation fosters AML cell proliferation and survival while impeding cell apoptosis. The results hold potential implications for targeting PD-L1 in AML treatment strategies.

Ovarian cancer is one of the most common malignant tumors in Gynecology, whose treatment was seriously limited by the unclear understanding of molecular mechanism in disease development. LncRNA FGFR3-AS1 is involved in human cancers. In this study, we aimed to clarify its regulatory effect on ovarian cancer.

Ovarian cell model was used in 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide (MTT) assay and flow cytometry for investigating the role of LncRNA FGFR3-AS1 in ovarian cancer. Western blot detection (CCND1、CDK6、MAPK9 and PIK3CA) tumor regulatory proteins. The study was conducted between March 2020 and October 2022 at General Hospital of Fushun Mining Bureau of Liaoning Health Industry Group, China.

The results demonstrated the upregulation of LncRNA FGFR3-AS1 in ovarian cancer, whose expression was positively related to tumor grade and AJCC stage, and negatively correlated with patients’ prognosis. LncRNA FGFR3-AS1 promoted ovarian cancer development through promoting cell growth and inhibiting cell apoptosis. PI3K signaling pathway-related proteins may be implicated in the LncRNA FGFR3-AS1 induced regulation of ovarian cancer.

LncRNA FGFR3-AS1 was involved in the development of ovarian cancer, which has the potential to become therapeutic target and prognostic indicator in ovarian cancer treatment.

Different kinds of treatments have been developed to fight cancers. Low-level laser therapy (LLLT), also known as photobiomodulation therapy (PBMT), is a low-power monochromatic and coherent light that has been used successfully for healing injuries and combating malignancies. However, there are concerns about the application of LLLT to cancers due to the increased proliferation of some cancer cells after LLLT.

This study investigated the effects of 650 nm and 870 nm lasers on the proliferation of HT29 colorectal cancer cell lines in vitro and in vivo.

The results showed that the laser with a wavelength of 870 nm did not meaningfully alter the proliferation of cultured cells. However, cell proliferation was promoted when the laser was applied within a wavelength of 650 nm. Treatment of HT29-derived tumors in nude mice with the 650 nm laser resulted in the decline of the tumor progression rate compared to controls. This result was inconsistent with the proliferative effects of the laser on the cultured cells.

Cell behavior in response to LLLT might be different between cell culture and xenograft models.

Statement of the Problem:

 Currently, the reconstruction of bone defects with new platelet concentrates is considered a significant challenge in periodontics.

This study aimed to evaluate advanced- platelet rich fibrin (A-PRF) and leukocyte- and platelet rich fibrin’s (L-PRF) effects on the proliferation and differentiation of MG-63 cells.

In this in vitro study, blood samples of five healthy non-smoking volunteers were collected and immediately centrifuged according to the two protocols of Choukroun and Ghanaati, without adding any anticoagulants, to prepare L-PRF and A-PRF. After freezing the clots for one hour, they were crushed and centrifuged once more. After culturing MG-63 cells, the effects of 20%, 10%, 1%, and 0.5% concentrations of A-PRF and L-PRF extracts on cell proliferation and mineralization were evaluated by methyl thiazolyl tetrazolium (MTT) assay and Alizarin Red staining, respectively.

Generally, survival and proliferation in the L-PRF group at both time intervals were higher than the A-PRF group and increased with increasing the extract concentration. However, in the A-PRF group, there were no significant differences between the different concentrations, and only the number of cells increased over time. After three days, in the study on mineralization, nodule formation was observed only in the positive control group (osteogenic). In seven days, mineralized nodules were formed in all groups with different concentrations of A-PRF, but not in any of the L-PRF groups.

According to the results, L-PRF increased proliferation, and A-PRF exerted a positive effect on the differentiation of MG-63 cells.

To explore Arsenic trioxide (As2O3) and its regulated miR-885-5p/CDC73 signaling pathway involved in the development of gastric cancer.

Fifty-two healthy patients and patients with gastric cancer were enrolled 2019-2020 in He Xian Memorial Hospital, Guangzhou, China. The patients with gastric cancer were divided into control group and As2O3 administration group. After 2 courses of treatment, their peripheral blood was collected to analyze the therapeutic effect. miR-885-5p expression in peripheral blood was analyzed by qRT-PCR. As2O3 was added into MGC-803 gastric cancer cell line at 0, 10, 20, 40 and 80 μmol/L. The proliferation rate and 48h IC50 value of gastric cancer cells were investigated by CCK-8, and the effect of As2O3 on miR-885-5p expression in the cells was analyzed.

After 4 weeks of treatment, the objective efficiency of control group and As2O3 administration group was 17.3% and 13.4%, respectively, without significant statistical difference. The overall benefit rate of As2O3 administration group was significantly higher than that of the normal treatment group (P=0.049). qRT-PCR experiment results found that miR-885-5p significantly highly expressed in peripheral blood in the As2O3 administration group, while miR-885-5p in gastric cancer was lower compared with normal people. Adding As2O3 to the gastric cancer cells could significantly inhibit miR-885-5p expression, while miR-885-5p in gastric cancer cells affected cell expression by targeted regulation, affecting cell proliferation.

As2O3 may be used as a drug treatment program for gastric cancer, and mainly regulates the proliferation of gastric cancer cells by affecting the miR-885-5p/CDC73 target axis to participate in the development of gastric cancer.

Spirulina platensis micro-algae have some effects on cellular procedures. The proliferative potential of mesenchymal stem cells (MSCs) will be decreased after repetitive passage.

The stromal cells were isolated, and then proven by differentiating to adipogenesis and osteoblastic lineage. The cell markers such as CD90 and CD105 were detected by flowcytometry. MSCs were treated with extract of S. platensis in logarithmic concentrations. MTT and ATP assays were done to determine cell proliferation capacity. The antioxidant and antimicrobial properties of the extract were evaluated.

The results obtained from differentiation confirm cells’ potential for osteoblastic and adipoblastic differentiation. Detection of CD90 and CD105 markers over 70% proved that the majority of cells are MSCs. Statistical analyzes revealed a significant increase in MSCs proliferation in the concentration of 0.9 µl/ml S. platensis. DPPH assay demonstrated that the extract could scavenge free radicals up to 57%. Additionally, the extract showed the inhibition zone up to 11 mm against a different strain of bacteria by agar well diffusion assay.

Secreting nutritional elements, S. platensis extract can be used as an antioxidant, antimicrobial, and growth agent for enhancing the proliferation of MSCs. Furthermore, the optimum concentration for cell treatment with S. platensis’s extract was investigated.

MicroRNA is a form of non-coding RNAs that able to regulate gene expression. miR-424 is one of the members of the regulatory family, which plays an important role in the proliferation and differentiation of myeloid cells. Epigenetic changes can change the level of miR-424 under environmental factors. Therefore, the level of expression of miR-424 in U937 cells of the myeloid line was evaluated in this research under the influence of vitamin D3 (VitD3) and retinoic acid (RA).

In this study, U937 cells were cultured in the presence of VitD3, and RA to evaluate cell proliferation, viability via the trypan blue exclusion test, and expression level of miR-424 by real-time PCR at specific times.

Cell proliferation has shown a significant decrease in the RA group versus other groups during incubation times (P < 0.05). In VitD3 group, there was a significant increase in cell proliferation after 24- and 48-hours incubation periods versus other groups. In the VitD3 and RA groups, the increase of cell proliferation caused the downregulation of miR-424. In addition, the upregulation of VitD3 group and downregulation of the RA group were significant versus the control group (P < 0.05).

We concluded that the expression level of miR-424 was critically affected in the dose- and time-dependent of RA and VitD3 treatment in the U937 cell line. Treatment with VitD3 decreased the expression of miR-424 and RA treatment increase miR-424 expression level in physiological doses.