Abstract
Cervical cancer is a prevalent female malignancy with poor survival rates. ARID1A is frequently mutated or deleted in a variety of tumors and YAP signaling is widely activated in human malignancies. Nevertheless, the mechanism of YAP signaling in ARID1A-mutated cervical cancer remains unknown. The cell viability was determined by MTT assay. The expression of ARID1A, YAP1 and CTGF were evaluated by western blot. The cell proliferation was detected by colony formation. The bioinformatics analysis suggested that mutation of ARID1A was associated with the activation of YAP1 signaling. In addition, knockdown of YAP1 inhibited ARID1A-mutated cervical cancer cells growth. Verteporfin is an inhibition of YAP1 signaling. Interestingly, knockdown of ARID1A decreased ARID1A-wildtype cervical cancer cells resistance to verteporfin. Meanwhile, overexpression of ARID1A increased ARID1A-mutated cervical cancer cells resistance to verteporfin. Similarly, blocking YAP1 signaling inhibited the tumor formation caused by ARID1A-mutated cervical cancer cells in vivo. Inhibition of YAP1 signaling suppresses ARID1A-mutated-induced tumorigenesis of cervical cancer, providing a novel therapeutic strategy for cervical cancer.
Highlights
Cervical cancer is a prevalent female malignancy with the highest mortality rate among all female malignant tumors [1, 2], and second highest in term of incidence among gynecological malignant tumors [3]
To explore the specific role of YAP1 in the context of ARID1A-mutated cervical cancers, two cell lines, C33A and CaSki, were regarded as ARID1A-mutated cell lines, in which ARID1A expression was severely reduced [14], whereas ME180 and HeLa cells served as wildtype cell lines
These results strongly suggested that loss of ARID1A in cervical cancer cells was mediated by the activation of YAP1 signaling
Summary
Cervical cancer is a prevalent female malignancy with the highest mortality rate among all female malignant tumors [1, 2], and second highest in term of incidence among gynecological malignant tumors [3]. In 2012, a total of 528,000 new cases and 266,000 deaths caused by cervical cancer were reported [4]. More than 80 percent of new cases are diagnosed in developing countries [5]. Due to advances in screening technologies and therapeutic strategies, the incidence and mortality of cervical cancer are declining [6]. The survival of cervical cancer patients is still poor [7]. It is urgent to uncover efficient diagnostic markers for cervical cancer
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