fig1

Novel players in the development of chemoresistance in ovarian cancer: ovarian cancer stem cells, non-coding RNA and nuclear receptors

Figure 1. (A) Apoptosis modulation to enhance chemoresistance in OC. The increased expression of Bcl-2, MCL-1, Bim, Bcl-XL, IAPs (Survivin, XIAP, &cIAP2), Bax phosphorylation and apoptosis regulation by ubiquitination, galectin, glycosylation, and epigenetic regulation inhibit apoptosis to confer chemoresistance in OC; (B) Increased DNA repair activity to enhance chemoresistance in OC. The aberrant expression of DNA repair genes, i.e., BRCA1/2, RAD51, and its paralogs RAD5IC and RAD5ID, RAD52, MRE11, RIFI, hMLH1, hMSIH2, ERCC1, XPF, RPA1, APE1, and XRCC1, promotes drug resistance in OC. Created with BioRender.com. OC: Ovarian cancer; Bcl-2: B cell lymphoma gene 2; MCL-1: myeloid cell leukemia sequence 1; IAPs: inhibitors of apoptosis proteins; X-linked inhibitor of apoptosis protein; BRCA 1/2: breast cancer gene 1/2; MRE11: meiotic recombination 11; hMLH1: human MutL homolog 1; hMSH2: human MutS homolog 2; ERCC1: excision repair cross-complementation group 1; XPF: xeroderma pigmentosum complementation group F; XRCC1: X-ray repair cross-complementing 1.

Cancer Drug Resistance
ISSN 2578-532X (Online)

Portico

All published articles will preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles will preserved here permanently:

https://www.portico.org/publishers/oae/