Ubiquitination of p53 is Involved in Troglitazone Induced Apoptosis in Cervical Cancer Cells

Chen, Huimin; Zhang, Dingguo; Wu, Jin-Xiz; Pei, Dong‐Sheng; Zheng, Jian

doi:10.7314/apjcp.2014.15.5.2313

Cited by 11 publications

(10 citation statements)

References 26 publications

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“…Regarding the roles of PPARγ in cervical cancer, one report shows that PPARγ is less abundant in cervical carcinoma tissues than in normal cervical tissues (18), which is confirmed in the present study. Another study showed that treatment with PPARγ agonist in vitro induced apoptosis and suppressed proliferation of cervical cancer cells (43). In this study, we found that the inhibition of PPARγ by siRNA promoted proliferation and invasion of cervical cancer cells, implicating the antitumor roles of PPARγ in cervical cancer.…”

Section: Discussionsupporting

confidence: 56%

Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells

Zhang

Liu

Mao

et al. 2015

International Journal of Oncology

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MicroRNAs (miRNAs) have been reported to be involved in multiple biological pathways that can influence tumor progression and metastasis. High-risk human papillomavirus (HR-HPVs) is aetiologically correlated to cervical cancer. Recently, miRNAs were reported to be regulated by virus and play pivotal roles in HPV-related tumor progression. However, the underlying mechanism remains poorly understood. In the present study, we report that HPV16 E7 upregulated miR-27b to promote proliferation and invasion in cervical cancer. The results showed that PPARγ, as a target of miR-27b, played a significant role in suppressing cervical cancer progression by downregulating the sodium-hydrogen exchanger isoform 1 (NHE1). It was also shown that the inhibition of miR-27b diminished the ability of HPV16 E7 to suppress PPARγ or activate NHE1 expression. In addition, we observed high expression of miR-27b and NHE1, but low expression of PPARγ in HPV16-positive cervical cancer tissues. In summary, the present study revealed that miR-27b is upregulated by HPV16 E7 to inhibit PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells.

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Section: Discussionsupporting

confidence: 56%

Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells

Zhang

Liu

Mao

et al. 2015

International Journal of Oncology

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“…Our results differ from those of Chen et al in human cervical cancer HeLa cells. 16 They demonstrated that TGZ induces apoptosis, which is closely related to p53 ubiquitin and the presence of the TGZ-PPARγ-p53 signaling pathway, and is a critical regulator of apoptosis. Differences in histopathology and genomics between human cervical cancer cell lines may result in different biological behavior.…”

Section: Discussionmentioning

confidence: 99%

Antiproliferative effects and molecular mechanisms of troglitazone in human cervical cancer in vitro

Ye¹,

Li²,

Xie³

et al. 2015

OTT

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We investigated the effects of troglitazone on human cervical cancer SiHa cells and its mechanisms of action. SiHa cells were incubated with different concentrations of troglitazone (100, 200, or 400 μg/mL) for 24, 48, and 72 hours. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay; cell cycle and apoptosis were detected by flow cytometry; and morphology of SiHa cells was observed under an inverted microscope. pcDNA3.1 and pcDNA3.1-Skp2 plasmids were constructed and then transfected into SiHa cells. Protein expression was analyzed by Western blotting. Troglitazone inhibited the proliferation of SiHa cells in a time- and concentration-dependent manner. Troglitazone caused G0/1 phase arrest but failed to reduce apoptosis in SiHa cells. Troglitazone significantly increased expression of p27 but decreased Skp2 expression. Skp2 overexpression inhibited the role of troglitazone in increasing expression of p27, and the cell cycle inhibitory effect of troglitazone. Troglitazone can inhibit SiHa cell viability by affecting cell cycle distribution but not apoptosis, and Skp2 and p27 may play a critical role.

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“…The resulting release of active E2F transcription factors leads to stimulation of S-phase cell cycle entry. E7 protein is found predominantly in the nucleus and to a minor extent in the cytoplasm in the cervical cancer cell line Ca Ski in vitro and in cervical carcinoma in situ, suggesting that nuclear resident E7 plays a major role in cervical carcinogenesis in humans (Fiedlwer M, 2004;Hui-Min Chen, 2014;Madhumita Roy, 2014) .The majority of Rb mutations lead to absence of Rb mRNA and its protein product. The complete absence of nuclear reactivity in all areas of tumour associated with a positive internal control has shown a strong indication of underlying Rb mutations (Noraini MD, 2003).…”

Section: Discussionmentioning

confidence: 99%

Significance of p53, pRb and Ki-67 markers in Cervical intraepithelial lesion and Malignancy

2015

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Abstract-Objective:To study and to derive the significance of expression of p53, pRb and Ki-67 markers in various grades of cervical intraepithelial lesions and malignancy in a tertiary hospital situated in southern part of India which caters the rural and semi-urban population.Methods: A total of 120 cervical tissue samples were included. These represented normal, dysplasia and malignancy. Immunohistochemical staining was performed for p53, Ki-67 and pRb in formalin-fixed, paraffin-embedded tissue sections of the uterine cervix using horse-peroxidase method. Descriptive statistical analysis was done; significance was assessed at 5% level of significance. The mean value of the markers was compared between normal and pathological lesions separately using Independent "t" test. Results: There was significant association of p53 expression between normal cervical epithelium and low grade squamous intraepithelial lesion (LSIL) (p=0.023), squamous cell carcinoma (SCC) (p<0.001) and adenocarcinoma AC (p=0.004), but no significant association with high grade squamous intraepithelial lesion (HSIL) (p=0.09). In case of pRb(n) (n=nuclear) expression significant association was found when normal was compared with LSIL (p<0.001) and HSIL (p=0.001), no association was found with SCC (p=0.207) and AC (p=0.322). pRb(c) (c=cytoplasmic) expression showed significant association when normal was compared with HSIL(p=0.03), SCC (p<0.001) and AC (p<0.001), but no association was found with LSIL. Whereas Ki-67 expression showed highly significant association with LSIL (p=0.012), HSIL (p<0.001), SCC (p<0.001) and AC (p<0.001). Conclusion: p53 expression progressively increased from normal cervical epithelium to intraepithelial lesion to malignant lesion. pRb expression showed shift of expression of pRb(n) in intraepithelial lesions to expression of pRb(c) in HSIL to frank malignancy. Ki-67 expression was directly proportional to the degree of dysplasia to malignant lesion.

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Ubiquitination of p53 is Involved in Troglitazone Induced Apoptosis in Cervical Cancer Cells

Cited by 11 publications

References 26 publications

Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells

Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells

Antiproliferative effects and molecular mechanisms of troglitazone in human cervical cancer in vitro

Significance of p53, pRb and Ki-67 markers in Cervical intraepithelial lesion and Malignancy

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