Therefore, our research revealed the mechanistic links between miR-744 and Bcl-2 in the pathogenesis of cervical cancer through modulation of Caspase-3, leading to the inhibition of cervical cancer cell growth.
The present study aimed to investigate the effect of ALA‑PDT on human cervical cancer through the regulation of microRNA‑143 (miR‑143) and the Bcl-2/Bax signaling pathway.
In the present study, we investigated the regulation by cisplatin on protein kinase C β (PKC β), on B-cell lymphoma 2 (Bcl-2) and on apoptosis in cervical cancer Hela cells.
Direct involvement in the regulation of Bcl-2 may be one of the mechanisms through which miR-143 may play a role in the pathogenesis of cervical cancer.
Our study suggests that coexpression of ER, PR, and bcl-2 may be a useful tool in identifying the CIN III lesions with low risk of progression to cervical cancer.
Immunohistochemical staining for bcl-2 protein (MoAB clone 124) was performed on operative tissue specimens from 22 patients with carcinoma in situ of the cervix and from 137 patients with invasive cervical carcinoma (International Federation of Gynecology and Obstetrics stages I to IV).
To analyze aberrant expression of the apoptotic protein p53 and the anti-apoptotic protein Bcl-2 in premalignant lesions of the uterine cervix induced by human papillomavirus (HPV) infection and its significance for early diagnosis of cervical cancer.
Our data demonstrated that leptin interferes with the expression of oncogenic c-myc and anti-apoptotic bcl-2, and regulates cell turnover and facilitates the progression of cervical cancer.
Moreover, the odds of being diagnosed with an invasive stage of cervical cancer were 3.7 times higher (95% CI, 1.6-8.8) for women positive for the E6 protein and 17 times higher (95% CI, 5.5-58.3) for women positive for the bcl-2 protein compared with women negative for E6 and bcl-2.
In conclusion, we consider that altered expression of Msh2, Mlh1, p53, and Bcl-2 may be a critical event during cervical cancer progression, whereas Fhit may be a component of a proapoptotic pathway.
As reported before, aberrant expression of proteins associated with signaling pathways, such as phosphatidylinositol 3-kinase(PI3K), EGF-R, β-catenin, and Erk and Bcl-2 was discovered in CC.
Analysis of the expression profile of Bcl-2 in cervical tissue revealed its up-regulation in cervical carcinoma, which agrees with results obtained from the in vitro data.
The up-regulation of Bcl2 and c-Met promotes the cervical cancer's progress, and the expression of miR-34a and miR-206 significantly correlated with the progression and prognosis in cervical cancer.
In endometrial carcinoma, bcl-2 and bcl-xL levels were correlated inversely (r = -0.27; P < .054), whereas in cervical cancer, they were correlated directly (r = +0.40; P < .002).
Mifepristone reversed the resistance of HeLa/MMC cells to MMC in vitro; the overexpression of the GCS gene and the increased expression of apoptosis-related protein Bcl-2 may play important roles in the formation of multidrug resistance in cervical cancer.
Deregulation of the apoptotic machinery plays a major role in cell death, cellular transformation and cancer. p53, Bcl-2, Bcl-XL, Bax and Mdm2 mRNA expression patterns were evaluated in tissue samples with cervical intraepithelial neoplasia (CIN) and cervical cancer compared to those of normal cervical tissues, and correlated with the underlying cervical lesions.