Long non-coding RNA cancer susceptibility candidate 2 inhibits the cell proliferation, invasion and angiogenesis of cervical cancer through the MAPK pathway.

Abstract

Increasing evidence has indicated that long non-coding RNA cancer susceptibility candidate 2 (CASC2) is aberrantly expressed and acts as a key regulator in various types of cancer. However, few reports have mentioned the precise function of CASC2 in cervical cancer. In the present study, CASC2 levels in cervical cancer tissues and cell lines were measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The proliferation, migration, and invasion of cervical cancer cells were detected by cell counting kit-8 (CCK-8) and transwell assays. Angiogenesis was evaluated by tube formation assays of human umbilical vein endothelial cells (HUVECs). The protein levels of the components of the mitogen-activated protein kinase (MAPK) pathway, including the c-Jun N-terminal kinase (JNK) and the extracellular-signal-regulated kinase-1 (ERK1), in cell lines of cervical cancer were detected by Western blot. CASC2 levels in human cervical cancer tissues and cell lines were significantly downregulated compared to para-cancerous tissues and the immortalized human keratinocyte line HaCaT. Compared to scramble group, CASC2 overexpression significantly inhibited the proliferation, migration, invasion, and angiogenesis of cervical cancer cells. However, the inhibition of CASC2 had the opposite effect. Moreover, the expression of p-JNK and p-ERK1 levels in the MAPK pathway was significantly decreased in pcDNA3.1-CASC2 group. Overexpression of CASC2 may inhibit the development of cervical cancer through the inactivation of the MAPK pathway and may be a potential therapeutic target for the treatment of patients with cervical cancer.