HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27

The main characteristics of cervical cancer are abnormal and uncontrolled cell proliferation, and it regulates cell growth, differentiation, and cell death through genetic and epigenetic changes. This paper mainly discusses the radiosensitivity of the cervical cancer protein kinase B signaling pathway and discusses the specific mechanisms that affect the occurrence and development of cervical cancer. In addition, this paper studies the effect of transient transfection knocking down the expression of TRIP4 in cervical cancer cells on the expression of key proteins in related signaling pathways and explores the mechanism of its specific effects and finds the mechanism of TRIP4’s effect on cervical cancer radiosensitivity. The findings of this study show for the first time that knocking down TRIP4 inhibits cell viability by inhibiting the P13K/AKT and MAPK/ERK pathways, and this corresponds to the first part of the experimental results, which show that knocking down TRIP4 inhibits colony formation and increases apoptosis in HeLa and SiHa cells. Moreover, simultaneous inhibition of TRIP4 and hTERT proteins can increase the radiosensitivity of cervical cancer cells. These findings indicate that the inhibition of TRIP4 may be a new type of treatment that selectively targets the P13K/AKT and MAPK/ERK pathways and hTERT pathways in cervical cancer cells and provides a therapeutic option for the treatment of cervical cancer.

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Isothiocyanates sensitize the effect of chemotherapeutic drugs via modulation of protein kinase C and telomerase in cervical cancer cells

Molecular and Cellular Biochemistry ◽

10.1007/s11010-009-0095-4 ◽

2009 ◽

Vol 330 (1-2) ◽

pp. 9-22 ◽

Cited By ~ 25

Author(s):

Sutapa Mukherjee ◽

Shubhabrata Dey ◽

R. K. Bhattacharya ◽

Madhumita Roy

Keyword(s):

Cervical Cancer ◽

Protein Kinase C ◽

Protein Kinase ◽

Cancer Cells ◽

Chemotherapeutic Drugs ◽

Kinase C ◽

Cervical Cancer Cells

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Inhibition of EGFR nuclear translocation attenuate radioresistance through decreased p-DNA-PK expression in cervical cancer cells.

Journal of Clinical Oncology ◽

10.1200/jco.2017.35.15_suppl.e17011 ◽

2017 ◽

Vol 35 (15_suppl) ◽

pp. e17011-e17011

Author(s):

Yunxiang Qi ◽

Jinyi Lang ◽

Lu Li ◽

Mei Feng ◽

Yecai Huang

Keyword(s):

Cervical Cancer ◽

Dna Damage ◽

Protein Kinase ◽

Cancer Cells ◽

Nuclear Translocation ◽

Dna Damage Repair ◽

Cervical Cancer Cell Line ◽

Phosphorylation Level ◽

Damage Repair ◽

Cervical Cancer Cells

e17011 Background: The commonly used treatment for cervical cancer is radiotherapy. However, the resistance to irradiation and metastasis at the advanced stage is a common reason for the poor prognosis and high mortality. This study was designed to elucidate the role of epidermal growth factor receptor (EGFR) nuclear translocation in radioresistance, and its correlation with DNA damage repair pathway in the cervical cancer cells. Methods: The dynamic expression of EGFR, DNA-dependent protein kinase (DNA-PK), PDK-1, PKN1 and their phosphorylation level in irradiated cervical cancer cell line CaSki at 0 10 20 40 minutes was determined by western blotting. Besides, nuclear localization signal (NLS) peptide inhibitor and control peptides was synthesized and treated cells before irradiation to elucidate the correlation between EGFR nuclear translocation and DNA damage repair after irradiation. Results: Expression of EGFR, protein kinase N1 (PKN1), and DNA-PK in nucleus was increased after irradiation in CaSki cells. Irradiation also enhanced the phosphorylation level of EGFR at Thr654, PKN1 at T774 and DNA-PK at T2609. Inhibition of EGFR nuclear translocation by NLS peptide decreased the expression level of EGFR and DNA-PK in the nucleus, and attenuated their phosphorylation process. Conclusions: EGFR nuclear translocation riggered by irradiation promoted DNA damage repair in irradiated cervical cancer cells. This work facilitated us to understand the possible molecular mechanism of the resistance to irradiation in the treatment of cervical cancer, providing a potentially potent clinical method to cancer therapy.

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Protein kinase C β inhibits autophagy and sensitizes cervical cancer Hela cells to cisplatin

Bioscience Reports ◽

10.1042/bsr20160445 ◽

2017 ◽

Vol 37 (2) ◽

Cited By ~ 7

Author(s):

Na Li ◽

Wei Zhang

Keyword(s):

Cervical Cancer ◽

Protein Kinase C ◽

Protein Kinase ◽

Cancer Cells ◽

Hela Cells ◽

B Cell Lymphoma ◽

Kinase C ◽

Cervical Cancer Cells ◽

Pkc Β ◽

Induced Apoptosis

Recently, autophagy has been indicated to play an essential role in various biological events, such as the response of cervical cancer cells to chemotherapy. However, the exact signalling mechanism that regulates autophagy during chemotherapy remains unclear. In the present study, we investigated the regulation by cisplatin on protein kinase C β (PKC β), on B-cell lymphoma 2 (Bcl-2) and on apoptosis in cervical cancer Hela cells. And then we examined the regulation by cisplatin on autophagy and the role of autophagy on the chemotherapy in Hela cells. In addition, the regulation of the PKC β on the autophagy was also investigated. Our results indicated that cisplatin promoted PKC β in Hela cells. The PKC β inhibitor reduced the cisplatin-induced apoptosis, whereas increased the cisplatin-induced autophagy in Hela cells. On the other side, the PKC β overexpression aggravated the cisplatin-induced apoptosis, whereas down-regulated the cisplatin-induced autophagy. Taken together, our study firstly recognized the involvement of PKC β in the cytotoxicity of cisplatin via inhibiting autophagy in cervical cancer cells. We propose that PKC β would sensitize cervical cancer cells to chemotherapy via reducing the chemotherapy induced autophagy in cancer cells.

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