LINC00659 Regulates Colorectal Cancer Migration and Invasion by Targeting miR-485-5p/HOXC13 Axis

Abstract

BackgroundLong noncoding RNA LINC00659 has been reported to be involved in the carcinogenesis and progression of colorectal cancer. However, the molecular mechanism remains ambiguous.MethodsIn this study, we found that HOXC13 expression was closely related with colorectal cancer and positively correlated with LINC00659 via bioinformatics analysis and clinical validation experiment. Meanwhile, miR-485-5p was identified as an overlapped target miRNA. To further dissect whether miR-485-5p and HOXC13 were involved in LINC00659 mediated colorectal cancer progression, we first established human in vitro models and demonstrated that LINC00659 could directly bind with miR-485-5p and knockdown of LINC00659 upregulated the expression of miR-485-5p. In addition, knockdown of LINC00659 inhibited the expression of HOXC13 by targeting miR-485-5p. Finally, we analyzed the effect of LINC00659/miR-485-5p/HOXC13 axis on tumor growth. Both animal model and in vitro model confirmed the anti-tumor effect of knockdown of LINC00659, which could suppress the colorectal cancer cell viability, migration and invasion by targeting miR-485-5p/HOXC13 axis. Results1. LINC00659 and HOXC13 are highly expressed in colorectal cancer cells.2. miRNA-485-5p is lowly expressed in colorectal cancer cells.3. LINC00659/miR-485-5p/HOXC13 axis is important for colorectal cancer cells.4. LINC00659 promotes tumor growth by sponging miR-485-5p.ConclusionsOur study uncovered a novel mechanism of LINC00659 in the progression of colorectal cancer and provided a potential strategy for the treatment and diagnose of colorectal cancer.

Identification of N6-Methyladenosine-Related Factors and the Prediction of the Regulatory Mechanism of Hair Follicle Development in Rex and Hycole Rabbits

“…Knockdown of METTL4 led to downregulation and inactivation of the INSR pathway [48], thereby regulating the IRS-1/PI3K/AKT pathway to improve insulin resistance [49]. In addition, AKT regulates the expression of the ETSI [50], TRPV3 [51,52], HOXC13 [53][54][55], and FGF5 [56][57][58] genes through the mTOR, mTOR/TGF-β/miR-181, HIF-1a/miR-485-5p, and ERK 1/2 /LIN28/let-7b signaling pathways, respectively.…”