Pivotal prognostic and diagnostic role of the long non‑coding RNA colon cancer‑associated transcript 1 expression in human cancer (Review)

Abstract

Long non-coding RNAs (lncRNAs) have been classically defined as regulatory RNA members >200 nucleotides in length, without detectable open-reading frames to encode proteins. Previous studies have demonstrated that lncRNAs serve critical roles in multiple cancer types. Colon cancer-associated transcript 1 (CCAT1), a novel cancer-associated lncRNA, is significantly overexpressed in a number of malignancies. Functionally, as an oncogenic lncRNA, CCAT1 is involved in proliferation, migration, cell cycle progression, apoptosis, chemoresistance and other biological processes of cancer cells through complex regulation mechanisms in the cytoplasm or nucleus. In clinical applications, CCAT1 is additionally positively associated with histological differentiation, tumour node metastasis stage, vascular invasion, overall survival and recurrence-free survival, which demonstrates its important role as a diagnostic and prognostic marker in cancer. The present review summarises the current research progress of the oncogenic potential and clinical uses of CCAT1 in various human cancer types.

Long Non-Coding RNA in the Pathogenesis of Cancers

“…CCAT1 is a newly discovered oncogenic lncRNA, 2628 bp in length, which is located on chromosome 8q24.21 [46,273]. CCAT1 is firstly found to be upregulated in colon cancer [274] and its expression is suggested to be epigenetically activated by c-Myc [46,275]. There are two isoforms of CCAT1: CCAT1-S and CCAT1-L. CCAT1-S is expressed in the cytoplasm, while CCAT1-L is exclusively expressed in the nucleus.…”

“…There are two isoforms of CCAT1: CCAT1-S and CCAT1-L. CCAT1-S is expressed in the cytoplasm, while CCAT1-L is exclusively expressed in the nucleus. CCAT1-S can be generated from CCAT1-L and there is a positive regulatory relationship between them [275]. CCAT1 is reported to be upregulated in many types of cancer, including CRC, LC, GC, HCC, ESCC, and acute myeloid leukemia (AML) [275,276].…”

“…CCAT1-S can be generated from CCAT1-L and there is a positive regulatory relationship between them [275]. CCAT1 is reported to be upregulated in many types of cancer, including CRC, LC, GC, HCC, ESCC, and acute myeloid leukemia (AML) [275,276]. Studies have shown that the expression of CCAT1 in CRC tissue and CRC cell lines is significantly increased than that in normal para-carcinoma or adjacent mucosa tissue and normal colon-derived cells [277,278,279,280,281].…”

“…Mechanistically, CCAT1 expression is considered to be associated with cell cycle, proliferation, apoptosis, migration, invasion, and EMT process in multiple cells [275]. Overexpression of CCAT1 promotes cell proliferation and invasion [284], while downregulation of CCAT1 inhibits cell proliferation, migration, and invasion, and results in cell cycle arrest in CRC cell lines [278,284,285].…”

Knockdown of lncRNA CCAT1 enhances sensitivity of paclitaxel in prostate cancer via regulating miR-24-3p and FSCN1

“…6,7 LncRNA colon cancer-associated transcript 1 (CCAT1) plays an important role in the prognosis and diagnosis of human cancers through regulating proliferation, migration, cell cycle progress, chemoresistance and other processes. 8 Moreover, a number of investigators have demonstrated CCAT1 as an oncogene in multiple cancers, such as gastric adenocarcinoma, ovarian cancer, nasopharyngeal carcinoma and lung adenocarcinoma. [9][10][11][12] Notably, Chen et al 13 have reported that CCAT1 contributes to migration and invasion in PCa cells.…”