jie liu

Extended endoscopic sinus surgery (EESS) can reduce the recurrence rate of chronic rhinosinusitis (CRS). The purpose of this study was to investigate the effect of the application of modified “protective middle turbinate-EESS” (mEESS) on patients with CRS with nasal polyps (CRSwNP) and allergic rhinitis (AR). Forty-three patients with CRSwNP and AR were classified into 2 groups, the mEESS group (n=23) and the functional endoscopic sinus surgery (FESS) group (n=20), and were followed up for 6 months and 1 year after surgery. The disease severity was assessed by the Lund-Mackay score, the Lund-Kennedy score, and the visual analog scale (VAS) score. The patency rate of the frontal sinus was evaluated by endoscopy. Patient satisfaction was also followed up. No preoperative differences or postoperative complications were found between the 2 groups. The VAS score and Lund-Kennedy score of the 2 groups were lower at 6 months and 1 year after surgery. The olfactory function of the mEESS group was significantly better than that of the FESS group at 6 months post-operative. The patency rate of the frontal sinus orifice in the mEESS group was significantly higher than that in the FESS group at 6 months and 1 year post-operative. Patient satisfaction in the mEESS group was relatively higher than that in the FESS group. mEESS improves frontal sinus drainage, olfactory sense, and patient satisfaction in the short term.

Reportedly, long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is involved in regulating colorectal cancer (CRC) progression. However, the function and detailed downstream mechanism of CASC2 in CRC progression are not fully elucidated. The aim of the study was to investigate the potential function and molecular mechanism of CASC2 in CRC progression.

In this experimental study, quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to probe CASC2, microRNA-18a-5p (miR-18a-5p) and B cell translocation gene 3 (BTG3) mRNA expression in CRC tissues and cell lines. After CASC2 was overexpressed in Colo-678 and HCT116 cell lines, methylthiazol tetrazolium (MTT) and 5-bromo-2’-deoxyuridine (BrdU) assays were employed to examine the proliferation of CRC cells. Transwell migration and invasion assays were executed to evaluate the metastatic potential of CRC cells. The targeting relationships among CASC2, miR-18a-5p and BTG3 were validated by dual luciferase reporter gene assay. Western blot assay was applied to examine the regulatory effects of CASC2 and miR-18a-5p on BTG3 protein expression.

CASC2 was decreased in CRC tissues and cell lines, and its low expression in CRC tissues was associated with larger tumor size and lymph node metastasis. CASC2 overexpression restrained proliferative, migrative and invasive capabilities of CRC cells. CASC2 could function as a molecular sponge for miR-18a-5p and repress the expression of miR-18a-5p. Furthermore, the inhibitory effects of CASC2 on the malignant phenotypes of CRC cells was counteracted by miR-18a-5p mimics. Additionally, CASC2 could positively regulate BTG3 expression via suppressing miR-18a-5p.

CASC2 inhibits CRC development by suppressing miR-18a-5p and raising BTG3 expression.