Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes

Halim, Talha Abdul; Farooqı, Ammad Ahmad; Zaman, Farrukh

doi:10.1186/1475-2867-13-61

Cited by 14 publications

(16 citation statements)

References 180 publications

(189 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…What’s more, COL1A1 is a fibril-forming collagen found in most connective tissues and is abundant in bone, cornea, dermis and tendon, and its expression level is closely related to epithelial-to-mesenchymal transition (EMT) [ 27 , 28 ]. While the EMT was known to be associated with radioresistance [ 29 – 31 ] and PI3K pathway [ 32 – 35 ]. Thus, these indicated that the radioresistance function of COL1A1 may be closely related to EMT.…”

Section: Discussionmentioning

confidence: 99%

Regulatory effects of COL1A1 on apoptosis induced by radiation in cervical cancer cells

Liu

Liao

2017

Cancer Cell Int

View full text Add to dashboard Cite

BackgroundCervical cancer is a common cancer of women in developing countries, and radiotherapy still remains its predominant therapeutic treatment. Collagen type I alpha 1 (COL1A1) has been shown to have a radioresistance effect in previous studies. However, such effect of COL1A1 has not yet been revealed in cervical cancer.MethodsExpression of COL1A1 in cervical cancer tissues and normal tissues was assessed by qRT-PCR and immunohistochemistry. The effect of COL1A1 on radioresistance of human cervical cancer cell lines HeLa and CaSki was assessed using the colony formation assay. Apoptosis alterations were analyzed by flow cytometry. In addition, western blotting was used assessed the alterations of several critical apoptosis and signaling pathway related proteins.ResultsThe expression of COL1A1 was significantly increased in cervical cancer tissues compared with normal tissues at the mRNA and protein level. Further, based on COL1A1 knock down and COL1A1 activation cell models, a negative correlation was observed between COL1A1 expression level and radiosensitivity. Moreover, the findings are further supported by apoptosis analysis that COL1A1 activation could inhibit the apoptosis of cervical cancer cells. Subsequently, a significantly decreased expression of p-AKT and Bcl-2, increased expression of Caspase-3 were observed in the LY294002 plus radiation group compared with radiation alone group, while these influences caused by LY294002 or X-ray radiation were reversed after COL1A1 activation.ConclusionsTo our knowledge, this is the only study to profile the mechanisms that COL1A1 plays a crucial role in cervical cells anti-apoptosis induced by radiation. Therefore, our identification of radioresistance-related COL1A1 in cervical cancer could be a starting point to explore the function of collagens, adding a new dimension to our understanding of the cervical cancer, assisting cancer biologists and clinical oncologists in novel therapeutic strategies.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-017-0443-5) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Regulatory effects of COL1A1 on apoptosis induced by radiation in cervical cancer cells

Liu

Liao

2017

Cancer Cell Int

View full text Add to dashboard Cite

show abstract

“…Recent studies indicate the existence of an intricate HPV interactome, i.e., a network of intermolecular interactions of Е6 and Е7 with the host cell proteins [28]. By these interactions, the Е6 and Е7 proteins can modulate the profile of gene expression, host cell proteome, and intracellular signaling pathways (including MAPK-, Wnt-, Akt-, Notch-, mTORC-, and STAT-dependent cascades), leading to remodelling of epithelial cells [29].…”

Section: Main Textmentioning

confidence: 99%

RETRACTED ARTICLE: Molecular mechanisms in progression of HPV-associated cervical carcinogenesis

Gupta

Mania‐Pramanik

2019

J Biomed Sci

View full text Add to dashboard Cite

Cervical cancer is the fourth most frequent cancer in women worldwide and a major cause of mortality in developing countries. Persistent infection with high-risk human papillomavirus (HPV) is a necessary cause for the development of cervical cancer. In addition, genetic and epigenetic alterations in host cell genes are crucial for progression of cervical precancerous lesions to invasive cancer. Although much progress has been made in understanding the life cycle of HPV and it’s role in the development of cervical cancer, there is still a critical need for accurate surveillance strategies and targeted therapeutic options to eradicate these cancers in patients. Given the widespread nature of HPV infection and the type specificity of currently available HPV vaccines, it is crucial that molecular details of the natural history of HPV infection as well as the biological activities of viral oncoproteins be elucidated. A better understanding of the mechanisms involved in oncogenesis can provide novel insights and opportunities for designing effective therapeutic approaches against HPV-associated malignancies. In this review, we briefly summarize epigenetic alterations and events that cause alterations in host genomes inducing cell cycle deregulation, aberrant proliferation and genomic instability contributing to tumorigenesis.

show abstract

“…Viral oncoproteins have an important role in the regulation of signaling cascades that initiate responses that determine cell survival and promote the development of CC. Recent studies have revealed that E6 and E7 oncoprotein facilitated the β-catenin nuclear accumulation, leading the activation of Wnt/β-catenin signaling cascade and acceleration of cervical carcinogenesis by activating genes that induce an increase in cell proliferation [4, 5]. E7 oncogene also induces the nuclear translocation of Smad proteins in a ligand-independent manner and interacted with MH1 Domain of SMAD3 to repress its transcription through TGF-β [6, 7].…”

Section: Introductionmentioning

confidence: 99%

Interaction between 17β-estradiol, prolactin and human papillomavirus induce E6/E7 transcript and modulate the expression and localization of hormonal receptors

et al. 2019

View full text Add to dashboard Cite

Background Cervical cancer (CC) is the second most common cancer in less developed countries and the second leading cause of death by cancer in women worldwide. The 99% of CC patients are infected with the Human Papilloma Virus (HPV), being HPV16 and HPV18 infection the most frequent. Even though HPV is considered to be a necessary factor for the development of CC, it is not enough, as it requires the participation of other factors such as the hormonal ones. Several studies have demonstrated the requirement of estrogen and its receptors (ERα, ERβ, and GPER) in the precursor lesions progress towards CC. Also, prolactin (PRL) and its receptor (PRLR) have been associated with CC. The molecular mechanisms underlying the cooperation of these hormones with the viral oncoproteins are not well elucidated. For this reason, this study focused on analyzing the contribution of 17β-estradiol (E2), PRL, and HPV on the expression and localization of hormone receptors, as well as to evaluate whether these hormones may promote greater expression of HPV oncogenes and contribute to tumor progression. Methods qPCR was used to evaluate the effect of E2 and PRL on the expression of E6 and E7 oncoproteins in HeLa and SiHa cervical cancer cells lines. HaCaT cells were transduced with the viral oncogenes E6 and E7 from HPV 16 and 18. ERα, ERβ, GPER, and PRLR expression and localization were evaluated by qPCR, Western blot and immunofluorescence. Results E2 and PRL induce E6/E7 oncogenes expression in HeLa and SiHa cells. E6 and E7 oncogenes of HPV16/18 significantly increased the protein expression of ERα, GPER, and PRLR. ERβ was positively regulated only by E6 oncogenes of HPV16/18. Besides, some of these oncogenes modify the location of PRLR toward cytoplasm, and ERα, ERβ, and GPER mainly to the nucleus. Conclusion Our studies suggest that the mutual regulation between E2, PRL, and HPV oncogenes could cooperate with the carcinogenesis process in CC.

show abstract

Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes

Cited by 14 publications

References 180 publications

Regulatory effects of COL1A1 on apoptosis induced by radiation in cervical cancer cells

Regulatory effects of COL1A1 on apoptosis induced by radiation in cervical cancer cells

RETRACTED ARTICLE: Molecular mechanisms in progression of HPV-associated cervical carcinogenesis

Interaction between 17β-estradiol, prolactin and human papillomavirus induce E6/E7 transcript and modulate the expression and localization of hormonal receptors

Contact Info

Product

Resources

About