Abstract

X-inactive–specific transcript (XIST) is one of the firstly discovered long non-coding RNAs with prominent roles in the process of X inactivation. Moreover, this transcript contributes in the carcinogenic process in different tissues. In addition to interacting with chromatin modifying molecules, XIST can be served as a molecular sponge for miRNAs to modulate expression of miRNA targets. Most of the studies have indicated an oncogenic role for XIST. However, in prostate cancer, a single study has indicated a tumor suppressor role for this lncRNA. Similar result has been reported for XIST in oral squamous cell carcinoma. In hepatocellular carcinoma, breast cancer, ovarian cancer, osteosarcoma, and renal cell carcinoma, different studies have reported inconsistent results. In the present manuscript, we review function of XIST in the carcinogenesis.

Highlights

  • X-inactive–specific transcript (XIST) RNA is among the firstly discovered long non-coding RNAs in humans (Brown et al, 1992)

  • Animal studies in hepatocellular carcinoma, breast cancer, ovarian cancer and osteosarcoma have indicated inconsistent results regarding the role of XIST (Table 1)

  • Experiments in clinical samples obtained from patients have shown that expression of XIST is principally increased in tumoral samples compared with nearby non-cancerous samples (Supplementary Table 2)

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Summary

Introduction

X-inactive–specific transcript (XIST) RNA is among the firstly discovered long non-coding RNAs (lncRNAs) in humans (Brown et al, 1992). Liu et al (2020) have reported down-regulation of XIST and UBAP1 in breast cancer cells. XIST functions as a sponge for miR-200c-3p, which regulates expression of ANLN (Zhang et al, 2020). Both XIST silencing and miR-132 over-expression could inhibit gastric cancer cell proliferation and migration (Li et al, 2020a).

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