LncRNA MIAT Promotes the Proliferation and Invasion of Colorectal Cancer via Suppressing Apoptosis and Senescence

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Article Type:
Research/Original Article (دارای رتبه معتبر)
Abstract:
Background
Myocardial infarction-associated transcript (MIAT) is a long noncoding RNA (lncRNA), which functions in a variety of disorders, like myocardial infarction and diabetic retinopathy. Moreover, recent reports have established that MIAT is upregulated in several types of malignancies and plays a crucial role in tumorigenesis. Therefore, this research aimed to investigate the expression of MIAT in colorectal cancer (CRC) and further evaluate the impact of its knocking-down on the proliferation and migration of the CRC cell.
Method
In this case-control experimental study, we evaluated the expression level of MIAT in a series of CRC and marginal tissues using RT-qPCR. Furthermore, the role of MIAT was assessed employing RNA interference (RNAi)-mediated suppressing strategy in CRC-derived cells. Subsequently, colony formation, cell cycle analysis, migration, apoptosis, and senescence assays were done to decipher the influence of MIAT on initiation and progression of CRC.
Results
Our findings revealed that MIAT expression is significantly upregulated in high-grade and vascular invasion tumor tissues. Furthermore, MIAT silencing led to G1 arrest in SW116 and SW48 CRC-derived cells. We also found that MIAT inhibition contributed to the induction of apoptosis/cellular senescence as well as the limitation of colony formation capability and cell migration in CRC cells. The obtained findings also showed that MIAT silencing dysregulated the expression of ATM and CHK2 genes known as DNA damage responsive genes.
Conclusion
The results of the present study demonstrated that lncRNA MIAT may control CRC cell proliferation and metastasis through regulating DNA damageresponsive pathway and can be noticed as a potential marker for diagnosis, prognosis, and targeted-therapy of high-grade CRC.
Language:
English
Published:
Middle East Journal of Cancer, Volume:14 Issue: 2, Apr 2023
Pages:
219 to 229
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