Adenovirus type 12 E1B 55-kilodalton oncoprotein promotes p53-mediated apoptotic response of ovarian cancer to cisplatin

Wang, Junnai; Gao, Qinglei; Li, Qiang

doi:10.1007/s13277-015-3351-0

Cited by 2 publications

(2 citation statements)

References 28 publications

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“…let-7d also inhibits cell growth, metastasis and macrophage infiltration through targeting collagen, type III, α 1 and C-C motif chemokine ligand 7 in renal cell carcinoma (42). Additionally, p53 can activate cell-cycle arrest and cell apoptosis, when it is in a stable state, mediate apoptotic response and affect cisplatin resistance in OC (43,44). Furthermore, p53 mutation is known as a genetic event that exists in OC and associates notably with resistance to platinum-based chemotherapy (45).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA let‑7d‑5p rescues ovarian cancer cell apoptosis and restores chemosensitivity by regulating the p53 signaling pathway via HMGA1

Chen

Ren

et al. 2019

Int J Oncol

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Ovarian cancer (OC) is the gynecological malignancy type with the highest mortality rate in females. The regulatory effect of microRNAs (miRs) on their target genes serves a key role in tumor development. Therefore, in the present study, whether miR let-7d-5p targeting high mobility group A1 (HMGA1) regulated biological characteristics and chemosensitivity of OC cells by mediating the p53 signaling pathway was investigated. The let-7d-5p level was detected in OC tissues and adjacent normal tissues, followed by detection in OC cell lines SKOV3, A2780, OVCAR-3 and CaOV3, and human normal ovarian epithelial cell line (IOSE-80), in order to select the OC cell line for the following experiments. Subsequently, OC cells were treated with the let-7d-5p mimic, siHMGA1 and Tenovin-1. The targeting association between let-7d-5p and HMGA1 was then examined, and the OC cell viability, migration, cycle and apoptosis were evaluated. Subsequently, the chemosensitivity of OC cells to cisplatin was verified. Finally, expression levels of let-7d-5p, HMGA1, p21, B-cell lymphoma-2 (Bcl-2)-associated X (Bax), p27, p53 wild-type (p53 wt ), p53 mutated (p53 mut ), proliferating cell nuclear antigen (PCNA), cyclin-dependent kinase 2 (CDK2), matrix metallopeptidase (MMP)2, MMP9 and Bcl-2 were determined. As demonstrated in the results, let-7d-5p expression was low in OC tissues and had an increased reduction in the OVCAR-3 cell line. HMGA1 was confirmed as a target of let-7d-5p, and its expression was also silenced by let-7d-5p. let-7d-5p repressed OC cell viability, migration, cell cycle progression and apoptosis, while it promoted the chemosensitivity of OC cells to cisplatin by targeting HMGA1. The expression of let-7d-5p, p21, Bax, p27 and p53 wt was increased, while that of HMGA1, p53 mut , PCNA, CDK2, MMP2, MMP9 and Bcl-2 was reduced following cell transfection. The results in the present study provided evidence that let-7d-5p may suppress proliferation, and facilitate apoptosis and cisplatin chemosensitivity of OC cells by silencing HMGA1 via the p53 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

MicroRNA let‑7d‑5p rescues ovarian cancer cell apoptosis and restores chemosensitivity by regulating the p53 signaling pathway via HMGA1

Chen

Ren

et al. 2019

Int J Oncol

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“… 46 The AD type 12 E1B 55-kilodalton oncoprotein tightly associates with P53, and accelerates P53-mediated apoptosis response of OC to cisplatin. 47 …”

Section: Advances In New Strategies In Targeting P53 For Ovarian Cancmentioning

confidence: 99%

Cellular Mechanism of Gene Mutations and Potential Therapeutic Targets in Ovarian Cancer

Guo

Xue

Xie³

et al. 2021

CMAR

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Ovarian cancer is a common and complex malignancy with poor prognostic outcome. Most women with ovarian cancer are diagnosed with advanced stage disease due to a lack of effective detection strategies in the early stage. Traditional treatment with cytoreductive surgery and platinum-based combination chemotherapy has not significantly improved prognosis and 5-year survival rates are still extremely poor. Therefore, novel treatment strategies are needed to improve the treatment of ovarian cancer patients. Recent advances of next generation sequencing technologies have both confirmed previous known mutated genes and discovered novel candidate genes in ovarian cancer. In this review, we illustrate recent advances in identifying ovarian cancer gene mutations, including those of TP53, BRCA1/2, PIK3CA, and KRAS genes. In addition, we discuss advances in targeting therapies for ovarian cancer based on these mutated genes in ovarian cancer. Further, we associate between detection of mutation genes by liquid biopsy and the potential early diagnostic value in ovarian cancer.

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Adenovirus type 12 E1B 55-kilodalton oncoprotein promotes p53-mediated apoptotic response of ovarian cancer to cisplatin

Cited by 2 publications

References 28 publications

MicroRNA let‑7d‑5p rescues ovarian cancer cell apoptosis and restores chemosensitivity by regulating the p53 signaling pathway via HMGA1

MicroRNA let‑7d‑5p rescues ovarian cancer cell apoptosis and restores chemosensitivity by regulating the p53 signaling pathway via HMGA1

Cellular Mechanism of Gene Mutations and Potential Therapeutic Targets in Ovarian Cancer

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