Involvement of p53-dependent apoptosis signal in antitumor effect of Colchicine on human papilloma virus (HPV)-positive human cervical cancer cells.

Abstract

Colchicine, a plant-derived alkaloid with relatively low toxicity on normal human epidermal keratinocytes (HEKn), has selective inhibitory effect on the growth of CaSki (HPV16-positive) and HeLa (HPV18-positive) human cervical cancer cell lines via the induction of apoptosis. Colchicine (2.5, 5.0 and 10.0 ng/ml) significantly reduced the expression of human papilloma virus (HPV) 16 E6/E7 mRNA and protein in CaSki and HeLa cells. Moreover, reduced expression of E6 and E7 induced by Colchicine resulted in the up-regulation of tumor suppressor proteins, p53 and Rb, as well as down-regulation of phospho Rb (pRb) protein. In addition, Bax, cytosolic cytochrome c and cleaved caspase-3 protein were increased while Bcl-2 protein was decreased significantly by 48 h of Colchicine treatment. These results implied that Colchicine could be explored as a potent candidate agent for the treatment and prevention of HPV-associated cervical cancer without deleterious effects.

• Authors: Luchun Yan, Hao Huang, Ying Zhang, Xinrong Yuan, Zhaohua Yan, Chunyan Cao, Xiping Luo
• Journal: Bioscience reports (Biosci Rep) Vol. 40 Issue 3 (03 27 2020) ISSN: 1573-4935 [Electronic] England
• PMID: 32163135 (Publication Type: Journal Article)
• Copyright: © 2020 The Author(s).

Chemical References

• E6 protein, Human papillomavirus type 16
• Oncogene Proteins, Viral
• Papillomavirus E7 Proteins
• Repressor Proteins
• Retinoblastoma Protein
• TP53 protein, human
• Tumor Suppressor Protein p53
• oncogene protein E7, Human papillomavirus type 16
• Colchicine

Topics

• Apoptosis (drug effects)
• Colchicine (pharmacology)
• Female
• HeLa Cells
• Human papillomavirus 16 (genetics, isolation & purification)
• Humans
• Oncogene Proteins, Viral (biosynthesis, metabolism)
• Papillomaviridae (drug effects, isolation & purification, metabolism)
• Papillomavirus E7 Proteins (biosynthesis, metabolism)
• Papillomavirus Infections (metabolism, pathology)
• Repressor Proteins (biosynthesis, genetics, metabolism)
• Retinoblastoma Protein (biosynthesis, genetics)
• Tumor Suppressor Protein p53 (genetics, metabolism)
• Uterine Cervical Neoplasms (drug therapy, metabolism, pathology, virology)