Abstract
Long non-coding RNA (lncRNA) PCAT6 is a member of the Prostate Cancer Associated Transcripts family of molecules. In this review, we focus on the latest studies involving PCAT6 in the diagnosis, treatment, and prognosis of malignant tumors of the digestive, respiratory, urinary, reproductive, motion, and nervous systems. PCAT6 was found to be highly expressed in gastric cancer, colon cancer, hepatocellular carcinoma, lung cancer, bladder cancer, ovarian cancer, breast cancer, cervical cancer, osteosarcoma, glioblastoma, and other tumors. PCAT6 can promote the development and progression of different types of malignant tumors through various mechanisms. Overall, these findings suggest that PCAT6 may play an increasingly vital role in the clinical assessment of these malignant tumors. It can function as an oncogene and may be used as a potential new prognostic biomarker of these tumors.
Highlights
According to the human genome project, protein-coding genes account for less than 2% of the entire genome, while the remaining DNA is non-coding
Kaplan-Meier analysis indicated that patients with lower Prostate Cancer Associated Transcript 6 (PCAT6) expression levels had significantly longer overall survival (OS) (P < 0.001) and disease-free survival (DFS) (P < 0.05), suggesting that PCAT6 overexpression is correlated with poor prognosis of hepatocellular carcinoma (HCC) patients [31]
Kaplan-Meier analysis revealed that bladder cancer (BC) patients with low PCAT6 expression showed longer OS times compared with those patients with high PCAT6 expression. These results indicate that upregulated PCAT6 could predict poor prognosis in BC patients
Summary
According to the human genome project, protein-coding genes account for less than 2% of the entire genome, while the remaining DNA is non-coding. Knockdown of PCAT6 could regulate miR-330-5p, resulting in inhibited proliferation, migration, and invasion of NSCLC cell lines. QRT-PCR analysis revealed that the expression levels of PCAT6 were significantly upregulated in 20 GC tissues compared with those in paired adjacent normal tissues. Immunoblotting and chemoresistance mechanistic studies have suggested that the elevated PCAT6 levels inhibit miR‐204 expression in CRC, promoting HMGA2/ PI3K signaling pathway activity and enhancing the chemoresistance of CRC cells to 5‐fluorouracil (FU) [28]. TOP/FOP flash reporter assays and qRTPCR analyses suggested that PCAT6 positively regulates the Wnt/b-catenin signaling pathway in CC cell lines by promoting the expression of c-myc, cyclin D1, and b-catenin [45]. Mechanistic studies revealed that PCAT6 can increase ZEB1 levels by sponging endogenous miR-143-3p, and the upregulation of ZEB1 can aggravate the malignant phenotype of osteosarcoma cells. Like colony formation, JC‐1, and sphere formation assays, revealed the importance of PCAT6 in promoting cell proliferation and stemness, as well as repressing cell apoptosis
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