Mutant p53 (p53-R248Q) functions as an oncogene in promoting endometrial cancer by up-regulating REGγ

Wang, Huihui; Bao, Wei; Jiang, Feizhou; Che, Qi; Chen, Zheng; Wang, Fangyuan; Tong, Huan; Dai, Chenyun; He, Xiaoyun; Liao, Yun; Liu, Binya; Sun, Jing; Wan, Xiaoping

doi:10.1016/j.canlet.2015.02.028

Cited by 49 publications

(34 citation statements)

References 55 publications

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“…Furthermore, mutant p53 may function as an oncogene to stimulate cell division and promote the growth of tumor cells (25). The results of the present study indicated that with the increase of OSCC pathological grading, mutant p53 positive rate was also increased, which was consistent with the results of previous studies (26)(27)(28)(29)(30)(31)(32), suggesting that the mutation of p53 may be significant in the pathological differentiation of OSCC. The negative correlation detected between the mutant p53 expression and the therapeutic efficacy indicated that mutant p53 may be used to predict the sensitivity of OSCC to 5-Fu and carboplatin chemotherapy.…”

Section: Discussionsupporting

confidence: 91%

Expression of mutant p53 in oral squamous cell carcinoma is correlated with the effectiveness of intra-arterial chemotherapy

Zhang

2015

Oncology Letters

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Abstract. The aim of the present study was to evaluate the correlation between the positive expression rate of mutant p53 and the clinical characteristics of patients with oral squamous cell carcinoma (OSCC), as well as the effectiveness of intra-arterial chemotherapy. Expression of mutant p53 in tumor tissues was determined by immunohistochemical analysis of 51 OSCC patients, prior to and following intra-arterial chemotherapy. Prior to intra-arterial chemotherapy, mutant p53 positive rates in patients with higher pathological grades were significantly higher than those of the patients with lower pathological grades. The mutant p53 positive rate in patients with lymph node metastasis was 73% (19/26), which was significantly higher than that of the patients without lymph node metastasis (20%, 5/25). Mutant p53 was expressed in 17% (3/18) of clinical phase II patients, while 64% (21/33) of clinical phase III and IV patients exhibited positive expression of mutant p53 (P<0.05). The mutant p53 positive rate in chemotherapy non-responsive patients was 69% (11/16), which was significantly higher than that in the chemotherapy-responsive patients (37%, 13/35). Mutant p53 positive rates were not significantly correlated with age, gender or the location of the tumor. The mutant p53 positive rate prior to chemotherapy was 47% (24/51), and decreased to 18% (9/51) following chemotherapy. Expression of mutant p53 was decreased in all 13 (100%) chemotherapy-responsive patients, while only 5 (45%) chemotherapy non-responsive patients exhibited reduced expression levels of mutant p53 (P<0.05). In conclusion, mutant p53 has a significant role in the differentiation, development and treatment guidance of OSCC. Intra-arterial chemotherapy with 5-fluorourcil and carboplatin potentially exerts a therapeutic effect by reducing the expression of mutant p53.

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Section: Discussionsupporting

confidence: 91%

Expression of mutant p53 in oral squamous cell carcinoma is correlated with the effectiveness of intra-arterial chemotherapy

Zhang

2015

Oncology Letters

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“…For each antibody, negative control studies were performed without the primary antibody. Previous reports confirmed that these antibodies showed immunoreactivity for each protein in EC [13,14] . The percentage of positive cells was scored as follows: 1, less than 1% of the nuclei stained; 2, 1-10% of nuclei stained; 3, 10-33% of the nuclei stained; 4, 34-66% of nuclei stained; and 5, more than 67% of the nuclei stained.…”

Section: Immunohistochemical Staining and Interpretationsupporting

confidence: 71%

Small Foci of Serous Component as a Predictor of Recurrence and Prognosis for Stage IA Endometrial Carcinomas

Miyamoto

Takano²,

Tsuda³

et al. 2017

Oncology

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Objective: Most of the endometrial carcinomas are detected in early stages and have a better prognosis; however, predictive factors for recurrence have not been determined. Methods: Patients with grade 1 endometrioid carcinoma (EG1) according to the 2014 WHO criteria at FIGO 2009 stage IA that were identified through scanning medical charts were included, and we assessed whether the presence of uterine serous carcinoma (SC) component which comprised less than 5% of the total volume using the ovarian two-tiered grading system could be a recurrent risk factor in these patients. Results: Among 126 cases which met inclusion criteria, 12 cases had SC. SC tumors were divided into 2 groups: SC resembling high-grade serous carcinoma (HGSC) and SC resembling low-grade serous carcinoma (LGSC). Five (3.9%) cases had HGSC and 7 (5.6%) cases had LGSC. Recurrence was observed in 3 of all cases (2.3%): 2 cases with HGSC, and 1 case with LGSC. Regarding several clinicopathological factors, only the presence of SC was associated with recurrence. The sensitivity and specificity to predict recurrence using this system were 100 and 93%, respectively. Conclusion: The identification of SC using the ovarian two-tiered grading system could be an accurate predictor of recurrence in stage IA EG1.

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“…REGϒ-associated proteasomes can degrade specific proteins like cell-cycle inhibitors in an ubiquitin and ATP-independent manner. In EC, mutant p53-R248Q can bind to the promoter of and upregulate the expression of REGϒ (247). Depletion of REGϒ in EC lines reduces cell proliferation, migration, and invasion where as expression of mutant p53-R248Q promotes EMT (247).…”

Section: Microenvironmental Regulation Of Emt In Cancers Of the Femalmentioning

confidence: 99%

“…In EC, mutant p53-R248Q can bind to the promoter of and upregulate the expression of REGϒ (247). Depletion of REGϒ in EC lines reduces cell proliferation, migration, and invasion where as expression of mutant p53-R248Q promotes EMT (247). Overexpression of p53-R248Q cannot restore REGϒ protein levels in REGϒ-depleted EC cells, hinting at an alternative mode in which the restoration of these cells’ malignant properties occurs (247).…”

Section: Microenvironmental Regulation Of Emt In Cancers Of the Femalmentioning

confidence: 99%

Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology

et al. 2017

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Epithelial-to-mesenchymal transition (EMT) is a physiological process that is vital throughout the human lifespan. In addition to contributing to the development of various tissues within the growing embryo, EMT is also responsible for wound healing and tissue regeneration later in adulthood. In this review, we highlight the importance of EMT in the development and normal functioning of the female reproductive organs (the ovaries and the uterus) and describe how dysregulation of EMT can lead to pathological conditions, such as endometriosis, adenomyosis, and carcinogenesis. We also summarize the current literature relating to EMT in the context of ovarian and endometrial carcinomas, with a particular focus on how molecular mechanisms and the tumor microenvironment can govern cancer cell plasticity, therapy resistance, and metastasis.

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Mutant p53 (p53-R248Q) functions as an oncogene in promoting endometrial cancer by up-regulating REGγ

Cited by 49 publications

References 55 publications

Expression of mutant p53 in oral squamous cell carcinoma is correlated with the effectiveness of intra-arterial chemotherapy

Expression of mutant p53 in oral squamous cell carcinoma is correlated with the effectiveness of intra-arterial chemotherapy

Small Foci of Serous Component as a Predictor of Recurrence and Prognosis for Stage IA Endometrial Carcinomas

Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology

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