RECK inhibits cervical cancer cell migration and invasion by promoting p53 signaling pathway

Abstract

The present study was conducted to investigate the effects of RECK on cervical cancer cell migration and invasion to help understand relevant molecular mechanisms. QRT-PCR and western blot were respectively utilized to examine the transcriptional and translational levels of RECK in cervical cancer cell lines (HELA and C33A) and normal cell line (H8). After transfection with RECK overexpressing vectors, the expression of RECK mRNA, RECK and p53 signaling pathway-related proteins (p21, p53, bcl-2, and Bax) in cervical cancer cells were respectively examined using qRT-PCR and western blot. Cervical cancer cell migration after transfection was detected by wound healing assay and transwell assay. RECK expression was much lower in cervical cancer cell lines compared with normal cell line. Results of wound-healing assay results indicated that RECK could inhibit cervical cancer cell migration, and transwell assay results demonstrated that cell invasion was suppressed by RECK overexpression. Furthermore, western blot indicated that the overexpression of RECK could promote the activation of p53 signaling pathway by influencing related protein expression; whereas its inhibition by PFT-α could antagonize the effect of RECK on migrative and invasive abilities of cervical cancer cells. RECK could inhibit the migration and invasion of cervical cancer cells by activating p53 signaling pathway.

Combined effect of recombinant human adenovirus p53 and curcumin in the treatment of liver cancer

“…EMT was also notably suppressed, as demonstrated by the downregulation of N-cadherin, snail and twist expression, which are well documented markers of EMT (37,38). (41,42), in addition to inhibiting cancer cell migration (43)(44)(45). TP53 activation has also been previously reported to serve an inhibitory role in the EMT process, in human oral mucosal fibroblasts and oral submucous fibrosis by downregulating N-cadherin expression (46) and in colorectal cancer cells by downregulating Snail expression (37), which are findings consistent with the results of the present study.…”

LncRNA SNHG8 accelerates proliferation and inhibits apoptosis in HPV‐induced cervical cancer through recruiting EZH2 to epigenetically silence RECK expression

“…27 As illuminated previously, RECK impaired the malignant development of several tumors including CC. [28][29][30] Moreover, the methylation of RECK in several cancers has certified to predict poor prognosis, [31][32][33] while the potential mechanism has not been discussed in detail. Consistently, our research also revealed the tumor inhibitor role of RECK in HPV-positive CC cells and the accumulated H3K27me in the RECK promoter.…”

Erianin inhibits human cervical cancer cell through regulation of tumor protein p53 via the extracellular signal‑regulated kinase signaling pathway

“…Additionally, the upregulation of p53 in cancer cells may prevent cancer cell proliferation by promoting cell cycle arrest and apoptosis ( 33 – 36 ). Liu et al ( 37 ) revealed that the p53 pathway in human cervical cancer cells is activated by reversion-inducing-cysteine-rich protein with Kazal motifs overexpression, which induces cancer cell apoptosis and reduces migration. In the present study, erianin treatment of HeLa cells could promote the activation of p53.…”