Effects and mechanisms of GSG2 in esophageal cancer progression

Geng, Changran; Wang, Qiang; Xing, Pengfei; Wang, Min; Tong, Shao-Dong; Zhou, Ju-Ying

doi:10.1007/s00432-022-04260-2

Cited by 1 publication

(1 citation statement)

References 35 publications

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“…Recently, Huang et al, demonstrated that GSG2 is involved in the development of ovarian cancer and has the potential to be a therapeutic target and prognostic indicator for ovarian cancer treatment [ 19 ]. Geng et al, reported that GSG2 knockdown significantly inhibited various malignant biological behaviors of esophageal cancer cells, such as inhibiting proliferation, reducing colony formation, promoting apoptosis, and blocking migration [ 20 ]. Li et al, revealed that GSG2 promoted tumor growth through regulating cell proliferation in hepatocellular carcinoma [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

GSG2 facilitates the progression of human breast cancer through MDM2-mediated ubiquitination of E2F1

et al. 2023

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Background Breast cancer (BC) has posed a great threat to world health as the leading cause of cancer death among women. Previous evidence demonstrated that germ cell-specific gene 2 (GSG2) was involved in the regulation of multiple cancers. Thus, the clinical value, biological function and underlying mechanism of GSG2 in BC were investigated in this study. Methods The expression of GSG2 in BC was revealed by immunohistochemistry (IHC), qPCR and western blotting. Secondly, the biological function of GSG2 in BC was evaluated by MTT assay, flow cytometry, Transwell assay and wound healing assay. Furthermore, the potential molecular mechanism of GSG2 regulating the progression of BC by co-immunoprecipitation (Co-IP) and protein stability detection. Results Our data indicated that GSG2 was frequently overexpressed in BC. Moreover, there was a significant correlation between the GSG2 expression and the poor prognosis of BC patients. Functionally, GSG2 knockdown inhibited the malignant progression of BC characterized by reduced proliferation, enhanced apoptosis and attenuated tumor growth. Migration inhibition of GSG2 knockdown BC cells via epithelial-mesenchymal transition (EMT), such as downregulation of Vimentin and Snail. In addition, E2F transcription factor 1 (E2F1) was regarded as a target protein of GSG2. Downregulation of E2F1 attenuated the promoting role of GSG2 on BC cells. Mechanistically, knockdown of GSG2 accelerated the ubiquitination of E2F1 protein, which was mediated by E3 ubiquitin ligase MDM2. Conclusions GSG2 facilitated the development and progression of BC through MDM2-mediated ubiquitination of E2F1, which may be a promising candidate target with potential therapeutic value.

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Section: Introductionmentioning

confidence: 99%