Linc00702 inhibits cell growth and metastasis through regulating PTEN in colorectal cancer

D. Yu, X.-Y. Wang, Z.-L. Jin

Department of Anal-Colorectal Surgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China. yanhuaxuhj@163.com

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• Oncology

OBJECTIVE: To elucidate the expression and influence of Linc00702 on the development and progression of colorectal cancer (CRC).

PATIENTS AND METHODS: The expression of Linc00702 was evaluated using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in 91 paired CRC tissue samples and adjacent normal tissue samples, as well as in CRC cell lines. Cell proliferation in Caco2 and SW620 cells was detected using colony formation assay and 5-Ethynyl-2’-deoxyuridine (EdU) assay. Wound-healing assay and transwell analysis were utilized to assess the abilities of cell migration and invasion. Western blot analysis was employed to further explore the underlying mechanism of Linc00702 in CRC.

RESULTS: Linc00702 was lowly expressed in CRC tissues and cells. Over-expression of Linc00702 reduced cell proliferation, migration, and invasion of Caco2 cells, while knockdown of Linc00702 promoted cell growth and metastasis of SW620 cells comparing to control group, relatively. PTEN was verified as the target for Linc00702 in CRC, and Linc00702 promoted PTEN expression to inhibit the PI3K/AKT pathway.

CONCLUSIONS: Linc00702 was downregulated in CRC and inhibited cell proliferation, migration, and invasion by repressing the PI3K/AKT pathway via promoting PTEN expression. This might provide a new target for the biological treatment for CRC.

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