Long non‐coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR‐31

Abstract

Laryngeal squamous cell carcinoma (LSCC) is one aggressive malignancy and accounts for 20% of all head and neck cancer. However, the role of LOC554202 in human LSCC remains unknown. The expression level of LOC554202 and miR-31 was detected in the LSCC tiussues by using qRT-PCR. Cell growth was measured by CCK-8 assay. Flow cytometry and matrigel-coated membrane was used to detect for cell cycle and invasion respectively. We indicated that lncRNA LOC554202 expression was overexpressed in LSCC tissues compared with the paired adjacent samples and higher LOC554202 expression was associated with the advanced stage. In addition, we demonstrated that the expression level of miR-31 was downregulated in LSCC tissues compared to the paired adjacent samples and lower miR-31 expression was correlated with the advanced stage. Moreover, the expression of miR-31 was negatively correlated with the expression of LOC554202 in LSCC tissues. Ectopic expression of LOC554202 promoted LSCC cell growth, cell cyle and cell invasion and overexpression of miR-31 inhibited LSCC cell growth, cell cyle and cell invasion. Elevated expression of LOC554202 suppressed miR-31 expression and promoted RhoA expression in LSCC cell, which was a direct target gene of miR-31. Furthermore, LOC554202 increased LSCC cell growth, cell cyle and cell invasion through suppressing miR-31 expression. These results suggested that LOC554202 acted as an oncogene in the development of LSCC.

Downregulation of the long non-coding RNA taurine-upregulated gene 1 inhibits glioma cell proliferation and invasion and promotes apoptosis

“…TUG1-knockdown has been associated with cell cycle arrest in G 0 /G 1 phase (14). Glioma has been reported to be the most common type of primary cerebral tumor (1).…”

The predictive value of lncRNA MIR31HG expression on clinical outcomes in patients with solid malignant tumors

“…LncRNA MIR31HG, locating at human chromosome 9p21.3 [40] with transcription regulated by methylation of the promoter region [27], was found aberrantly expressed in several types of cancers. Specifically, MIR31HG was found elevated expressed in breast cancer [13], cervical cancer [28], chordoma [16], osteosarcoma [15], lung cancer [2,23,41], OSCC [4], PDAC [7], VSCC [29] and LSCC [36,42,43]. Nevertheless, the expression levels of MIR31HG was reported down-regulated in triple-negative breast cancer (TNBC) cell lines of basal subtype [27], bladder cancer [26], gastric cancer [25], CRC [32,33], and HCC [6].…”

“…For example, MIR31HG could enhance proliferation, migration and invasion by up-regulating EZH2/miR-31 and then indirectly activating the oncogene RNF144B in chordoma [16]. Yang et al demonstrated that elevated MIR31HG could inhibit miR-31 expression, and increase RhoA in LSCC, and via which promote cell growth, cell cycle and invasion [43]. In addition to miR-31, other miRNAs were also identified to interact with MIR31HG in carcinogenesis.…”

Overexpression of cancer susceptibility candidate 2 inhibited progression of hepatocellular carcinoma cells

“…Accumulating evidence have verified that the abnormal expression of lncRNAs is associated with tumor initiation. For example, TUG1, overexpressed in oral squamous cell carcinoma cells (Yan, Wang, Yang, Lu, & Zhou, 2017) and BANCR, upregulated in colorectal cancer cells, were associated with poor prognosis (Shen, Bai, Luo, & Zhou, 2017). Similarly, numerous studies reported that lncRNAs, as ceRNAs for miRNA, played a significant role in modulating HCC cell tumorigenesis.…”