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Original Research

Open Access

Expressions of H2AX in cervical squamous carcinoma and their clinical significances

  • J.Y. Ruan1,2
  • Q. Zhu1,2
  • L. Mei1,2
  • H. Wang1,2,*,

1Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, China

2Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, China

DOI: 10.12892/ejgo3304.2017 Vol.38,Issue 1,February 2017 pp.65-68

Published: 10 February 2017

*Corresponding Author(s): H. Wang E-mail: wanghe_cd@126.com

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Abstract

Objective: To evaluate the expression and clinical significance of H2AX in cervical squamous carcinoma. Materials and Methods. The expression of H2AX in the cervical squamous carcinoma of 37 patients and in the normal cervical tissue of 15 patients was detected by immuneohistochemical method. Chi-square, correlation analysis, and Kaplan-Meier were utilized to analyze the data. Results: The positive expression rate of H2AX in cervical squamous carcinoma was higher than that in normal cervical tissues (p = 0.016) . The expression of H2AX was negatively correlated with FIGO staging, vaginal invasion, and parametrial infiltration (p < 0.05). Survival analysis showed the expression intensity of H2AX had no significant effect on the prognosis. Conclusion: H2AX was an anticancer protein for cervical squamous carcinoma.

Keywords

Cervical squamous carcinoma; H2AX; Phosphorylate; Immunohistochemistry.

Cite and Share

J.Y. Ruan,Q. Zhu,L. Mei,H. Wang. Expressions of H2AX in cervical squamous carcinoma and their clinical significances. European Journal of Gynaecological Oncology. 2017. 38(1);65-68.

URL:

https://www.ejgo.net/articles/10.12892/ejgo3304.2017

References

[1] West M.H., Bonner W.M.: “Histone 2A, a heteromorphous family of eight protein species”. Biochemistry, 1980, 19, 3238.

[2] Lu C., Zhu F., Cho Y.Y., Tang F., Zykova T., Ma W.Y., et al.: “Cell apoptosis: requirement of H2AX in DNA ladder formation, but not for the activation of caspase-3”. Mol. Cell. Biol., 2006, 23, l2l.

[3] Jia Y.G., Yang Y.M., Zuo B., Guo L.D., Lou J.Y.: “DNA damage response in ovarian clear cell adenocarcinoma”. Sichuan Da Xue Xue Bao Yi Xue Ban, 2012, 43, 331. [Article in Chinese]

[4] Gao Z., Zhuang L., Chen Y.: “Effect and mechanism of gefitinib inhibition on non-small cell lung cancer radiosensitivity of HCC827 and H358 cell lines”. Zhongguo Fei Ai Za Zhi, 2012, 15, 324. [Article in Chinese]

[5] Rothkamm K., Horn S.: “Gamma–H2AX as protein biomarker for radiationexposure”. Ann. Ist. Super Sanita, 2009, 45, 265.

[6] Redon C.E., Dickey J.S., Bonner W.M., Sedelnikova O.A.: “Gamma–H2AX as a biomarkerof DNA damage induced by ionizing radiation in human peripheral bloodlymphocytes and artificial skin”. Adv. Space Res., 2009, 43, 1171.

[7] Liu Y., Tseng M., Perdreau S.A., Rossi F., Antonescu C., Besmer P., et al.: Histone H2AX is a mediator of gastrointestinal stromal tumor cell apoptosis following treatment with imatinib mesylate”. Cancer Res., 2007, 67, 2685.

[8] Dickey J.S., Redon C.E., Nakamura A.J., Baird B.J., Sedelnikova O.A., Bonner W.M.: “H2AX: functional roles and potential applications”. Chromosoma, 2009, 118, 683.

[9] Parikh R.A., White J.S., Huang X., Schoppy D.W., Baysal B.E., Baskaran R., et al.: “Loss of distal 11 q is associatedwith DNA repair deficiency and reduced sensitivity to ionizing radiationin head and neck squamous cell carcinoma”. Genes Chromosomes Cancer, 2007, 46, 761.

[10] Bassing C.H., Chua KF., Sekiguchi J., Suh H., Whitlow S.R., Fleming J.C., et al.: “Increased ionizing radiationsensitivity and genomic instability in the absence of histone H2AX”. Proc. Natl. Acad. Sci. USA, 2002, 99, 8173.

[11] Olive P.L.: “Detection of DNA damage in individual cells byanalysis of histone H2AX phosphorylation”. Methods Cell. Biol., 2004, 75, 355.

[12] Yuan J., Adamski R., Chen J.: “Focus on histone variant H2AX: to be or not to be”. FEBS Lett., 2010, 584, 3717.

[13] Bartkova J., Rezaei N., Liontos M., Karakaidos P., Kletsas D., Issaeva N., et al.: “Oncogene-induced senescence ispart of the tumorigenesis barrier imposed by DNA damage checkpoints”. Nature, 2006, 444, 633.

[14] Kunos C.A., Radivoyevitch T., Pink J., Chiu S.M., Stefan T., Jacobberger J., Kinsella T.J.: “Ribonucleotide reductase inhibition enhances chemoradiosensitivity of humancervical cancers”. Radiat. Res., 2010, 174, 574.

[15] Ivashkevich A., Redon C.E., Nakamura A.J., Martin R.F., Martin O.A.: “Use of the γH2AX assay to monitor DNA damage and repair in translational cancer research”. Cancer Lett., 2012, 327, 123.

[16] Zolner A.E., Abdou I., Ye R.: “Phosphorylation of polynucleotide kinase/ phosphatase by DNA-dependent protein kinase and ataxiatelangiectasia mutated regulates its association with sites of DNA damage”. Nucleic Acids Res., 2011, 39, 9224.

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