Silencing of linc00337 inhibits proliferation, cell cycle progression, migration, and invasion of colorectal cancer cells through the MEK/ERK pathway

Colorectal Cancer

Wang ZG, et al. Eur Rev Med Pharmacol Sci 2020.


OBJECTIVE: To explore the expression and biological functions of linc00337 in colorectal cancer (CRC), as well as its underlying mechanism.

PATIENTS AND METHODS: The relative expression of linc00337 in 47 cases of CRC tissues and cells was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The si-linc00337 interference sequences were designed and transiently transfected into CRC cells. The interference efficiency was detected via qRT-PCR. Regulatory effect of linc00337 on proliferation of CRC cells was detected via colony formation assay. Cell cycle distribution and apoptosis rate after interference in linc00337 expression were determined using flow cytometry. Moreover, the effects of linc00337 knockdown on cell migration and invasion were detected using transwell assay. At last, the effect of si-linc00337 on the MEK/ERK signaling pathway was detected using Western blotting.

RESULTS: The results of qRT-PCR showed that among the 47 cases of CRC tissues, the expression of linc00337 was up-regulated in 40 cases. Similarly, it was highly expressed in CRC cell lines. The results of colony formation assay manifested that cell proliferation declined after interference in linc00337 expression. The results of flow cytometry and transwell assay showed that interference in linc00337 expression arrested the cell cycle in G1/G0 phase, increased the apoptosis rate, and inhibited the invasion and migration of CRC cells. According to the results of Western blotting, expressions of molecular markers in the MEK/ERK pathway after interference in linc00337 expression were significantly changed.

CONCLUSIONS: Linc00337 is up-regulated in CRC tissues and cells. Interference in linc00337 expression can inhibit cell proliferation, migration, and invasion and promote apoptosis through the MEK/ERK pathway.