Expression of HOXC10 gene regulates the growth and invasion of prostate cancer cells

  • Hongmei Song Department of Interventional Radiology, Shanghai Sixth People's Hospital East Affiliated to Shanghai University of Medicine and Health Science, Shanghai 201306, China.
  • Xuxiao Ye Department of Urology, Shanghai Sixth People's Hospital East Affiliated to Shanghai University of Medicine and Health Science, Shanghai 201306, China.
  • Tao Liang Department of Urology, Shanghai Sixth People's Hospital East Affiliated to Shanghai University of Medicine and Health Science, Shanghai 201306, China.
  • Dongliang Yan Department of Urology, Shanghai Sixth People's Hospital East Affiliated to Shanghai University of Medicine and Health Science, Shanghai 201306, China.
  • Zuowei Li Department of Urology, Shanghai Sixth People's Hospital East Affiliated to Shanghai University of Medicine and Health Science, Shanghai 201306, China.
DOI: https://doi.org/10.3329/bjp.v16i1.50244
Keywords: HOXC10 gene, Prostate cancer cell

Abstract

The present study was undertaken to decipher the role of HOXC10 gene in regulating the growth and metastasis of prostate cancer. The results revealed significant (p<0.05) up-regulation of HOXC10 gene in human prostate cancer tissues and cell lines. The silencing of HOXC10 transcript level significantly (p<0.05) inhibited the growth and colony formation of DU145 and 22Rv1 prostate cancer cells. The DAPI staining revealed that inhibition of DU145 and 22Rv1 prostate cancer cell viability was due to the induction of apoptosis. The transwell assay showed that HOXC10 significantly (p<0.05) inhibits the invasion of prostate cancer cells. The Western blotting revealed that HOXC10 gene exerts its effects via modulation of Ras/Raf/MEK/ERK signaling cascade. Collectively, the results point towards the therapeutic potential of HOXC10 in the treatment of prostate cancer.

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References

Akam M. Hox genes and the evolution of diverse body plans. Philos Trans R Soc Lond B Biol Sci. 1995; 349: 313-19.

Ansari KI, Hussain I, Kasiri S, Mandal SS. HOXC10 is over-expressed in breast cancer and transcriptionally regulated by estrogen via involvement of histone methylases MLL3 and MLL4. J Mol Endocrinol. 2012; 48: 61-75.

Arab-Bafrani Z, Shahbazi-Gahrouei D, Abbasian M, Fesharaki M. Multiple MTS assay as the alternative method to deter-mine survival fraction of the irradiated HT-29 colon cancer cells. J Med Sig Sensors 2016; 6: 112.

Bhatlekar S, Fields JZ, Boman BM. HOX genes and their role in the development of human cancers. J Mol Med. 2014; 92: 811-23.

Chen Q, Zheng PS, Yang WT. EZH2-mediated repression of GSK-3β and TP53 promotes Wnt/β-catenin signaling-dependent cell expansion in cervical carcinoma. Oncotargetics 2016; 7: 36115-29.

Di Vizio D, Morello M, Dudley AC, Schow PW, Adam RM, Morley S, Mulholland D, Rotinen M, Hager MH, Insabato L, Moses MA. Large oncosomes in human prostate cancer tissues and in the circulation of mice with metastatic disease. Am J Pathol. 2012; 181: 1573-84.

Favier B, Dolle P. Developmental functions of mammalian Hox genes. Mol Hum Reprod. 1997; 3: 115-31.

Feng X, Li T, Liu Z, Shi Y, Peng Y. HOXC10 up-regulation contributes to human thyroid cancer and indicates poor survival outcome. Mol Biosyst. 2015; 11: 2946-54.

Guo C, Hou J, Ao S, Deng X, Lyu G. HOXC10 up-regulation promotes gastric cancer cell proliferation and metastasis through MAPK pathway. Chin J Cancer Res. 2017; 29: 572-80.

Han H, Li H, Zhou J. Long non-coding RNA MIR503HG inhibits the proliferation, migration and invasion of colon cancer cells via miR-107/Par4 axis. Exp Cell Res. 2020; 395: 112205.

Hostikka SL, Gong J, Carpenter EM. Axial and appendicular skeletal transformations, ligament alterations, and motor neuron loss in Hoxc10 mutants. Int J Biol Sci. 2009; 5: 397-410.

Jin Z, Li H, Hong X, Ying G, Lu X, Zhuang L, Wu S. TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway. Cancer Cell Int. 2018; 18: 202.

Jolma A, Yan J, Whitington T, Toivonen J, Nitta KR, Rastas P, Morgunova E, Enge M, Taipale M, Wei G, Palin K. DNA-binding specificities of human transcription factors. Cell. 2013; 152: 327-39.

Lopez R, Garrido E, Vazquez G, Pina P, Perez C, Alvarado I, Salcedo M. A subgroup of HOX Abd-B gene is differentially expressed in cervical cancer. Int J Gynecol Cancer. 2006; 16: 1289-96.

Ma Y, Xu Y, Li L. SPARCL1 suppresses the proliferation and migration of human ovarian cancer cells via the MEK/ERK signaling. Exp Therap Med. 2018; 16: 3195-201.

Mallo M, Wellik DM, Deschamps J. Hox genes and regional patterning of the vertebrate body plan. Dev Biol. 2010; 344: 7-15.

Martinez P, Amemiya CT. Genomics of the HOX gene cluster. Comp Biochem Physiol B Biochem Mol Biol. 2002; 133: 571-80.

Mehtälä J, Zong J, Vassilev Z, Brobert G, Gabarró MS, Stattin P, Khanfir H. Overall survival and second primary malignancies in men with metastatic prostate cancer. PloS one. 2020; 2020.

Montagut C, Settleman J. Targeting the RAF–MEK–ERK path-way in cancer therapy. Cancer Lett. 2009; 283: 125-34.

Pathiraja TN, Nayak SR, Xi Y, Jiang S, Garee JP, Edwards DP, Lee AV, Chen J, Shea MJ, Santen RJ, Gannon F. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer. Sci Transl Med. 2014; 6: 229.

Pearson JC, Lemons D, McGinnis W. Modulating Hox gene functions during animal body patterning. Nat Rev Genet. 2005; 6: 893-904.

Pienta KJ, Esper PS. Risk factors for prostate cancer. Ann Intern Med. 1993; 118: 793-803.

Riverso M, Montagnani V, Stecca B. KLF4 is regulated by RAS/RAF/MEK/ERK signaling through E2F1 and pro-motes melanoma cell growth. Oncogene 2017; 36: 3322-33.

Schulze A, Harris AL. How cancer metabolism is tuned for proliferation and vulnerable to disruption. Nature 2012; 491: 364-73.

Scott MP. Vertebrate homeobox gene nomenclature. Cell 1992; 71: 551-53.

Shah N, Sukumar S. The Hox genes and their roles in oncogenesis. Nat Rev Cancer. 2010; 10: 361-71.

Van Oostveen JW, Bijl JJ, Raaphorst FM, Walboomers JJ, Meijer CJ. The role of homeobox genes in normal hematopoiesis and hematological malignancies. Leukemia 1999; 13: 1675-90.

Yu Y, Chang Z, Han C, Zhuang L, Zhou C, Qi X, Peng Z. Long non-coding RNA MINCR aggravates colon cancer via regulating miR-708-5p-mediated Wnt/β-catenin pathway. Biomed Pharmacother. 2020; 129: 110292.

Zhai Y, Kuick R, Nan B, Ota I, Weiss SJ, Trimble CL, Fearon ER, Cho KR. Gene expression analysis of preinvasive and invasive cervical squamous cell carcinomas identifies HOXC10 as a key mediator of invasion. Cancer Res. 2007; 67: 10163-72.

Zheng L, He H, Shen X, Sun Y. Centipede scolopendra suppresses cell growth in high-EGFR expression cell A431. Bangladesh J Pharmacol. 2017; 12: 299-307.

Published
2021-01-04
How to Cite
Song, H., X. Ye, T. Liang, D. Yan, and Z. Li. “Expression of HOXC10 gene regulates the growth and invasion of Prostate cancer Cells”. Bangladesh Journal of Pharmacology, Vol. 16, no. 1, Jan. 2021, pp. 19-26, doi:10.3329/bjp.v16i1.50244.
Issue
Vol 16 No 1 (2021)
Section
Research Articles

Copyright (c) 2021 Hongmei Song, Xuxiao Ye, Tao Liang, Dongliang Yan, Zuowei Li

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