| Literature DB >> 33276182 |
Xiangxuan Zhao1, Wei Sun2, Ying Ren2, Zaiming Lu2.
Abstract
Cervical cancer (CC) is one of most common malignancies affecting women worldwide. To date, surgical resection is the only effective radical remedy for CC at its early stages, while the prognosis of metastatic or recurrent CC is very poor. Dysfunction of the tumor suppressor p53 due to aberrant expression, post-translational modification, mutations, SNPs, and LOH as well as sequestration by viral antigens and MDM2/HDM2-mediated degradation is closely associated with the therapeutic insensitivity and relapse of many malignancies, including CC. Accumulating studies have demonstrated that restoration of p53 activity can induce cell cycle arrest and apoptosis, eliminate radio- and chemotherapy resistance, and inhibit tumor growth in CC cells. Therefore, activation of wild-type p53 as well as restoration of p53 function seems appealing as a therapeutic strategy. In this review, we focus on the potential roles of p53 reactivation in CC treatment and their underlying molecular mechanisms towards the development of novel therapies.Entities:
Keywords: Cervical cancer; Prognosis; Signaling pathway; Targeted therapy; p53
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Year: 2020 PMID: 33276182 DOI: 10.1016/j.critrevonc.2020.103182
Source DB: PubMed Journal: Crit Rev Oncol Hematol ISSN: 1040-8428 Impact factor: 6.312