Clinicopathological Significance of Vimentin and Cytokeratin Protein in the Genesis of Squamous Cell Carcinoma of Cervix

Abstract

Cervical cancer is one of the commonest types of cancers worldwide especially in developing countries. Intermediate filaments protein family has shown a role in the diagnosis of various cancers, but a few studies are available about the vimentin and cytokeratin roles in the cervical cancer. This case control study aimed to interpret the expression of vimentin and cytokeratin proteins in the development and progression of cervical cancer and its correlation with clinicopathological features. The cytoplasmic expression of vimentin was observed in 40% of cases, but not in inflammatory lesions of cervix. It was noticed that vimentin expression was increasing significantly with high grade of the tumour. Cytokeratin expression was observed in 48.33% and it was noticed that the expression was 62.5% in well differentiated (G1), 45% in moderately differentiated (G2), and 41.66% in poorly differentiated carcinoma, yet statistically insignificant. The expression of vimentin and cytokeratin proteins was not significantly associated with age groups. The current findings concluded a possible role of vimentin in the development and progression of cervical cancer and vimentin marker will be useful in the diagnosis and grading of cervical cancer.

Research Article Vimentin is not a reliable prognostic biomarker for cervical cancer

“…The unusual expression of vimentina during reactivation of the EMT program in the invasion and metastasis process has already been investigated in several human tumors (Zhao et al, 2014;Holthoff et al, 2016;Figiel et al, 2017;Du et al, 2018). Regarding cervical cancer, there are still few studies evaluating the association of vimentin expression with prognostic aspects of tumors, especially with regard to survival and relapse-free interval evaluations Cheng et al, 2012;Yu et al, 2015;Husain et al, 2016;Lin et al, 2017).…”

“…The main risk factor for cervical cancer is persistent infection with human papillomavirus (HPV), mainly by genotypes 16 and 18 (Doobar, 2006). The expression of HPV oncoproteins leads to changes in tumor suppressor proteins such as p53 and retinoblastoma protein (pRb), altering the cell cycle and modifying a series of signaling pathways that favor tumor growth (Doorbar, 2006;McCloskey et al, 2010;Monsonego et al, 2011;Husain et al, 2016). With progression of the disease, tumor cells rupture the basal membrane of the epithelium, leading to growth of the primary tumor and its subsequent spread to distant tissues resulting in invasion and metastasis (Husain et al, 2016).…”

“…The expression of HPV oncoproteins leads to changes in tumor suppressor proteins such as p53 and retinoblastoma protein (pRb), altering the cell cycle and modifying a series of signaling pathways that favor tumor growth (Doorbar, 2006;McCloskey et al, 2010;Monsonego et al, 2011;Husain et al, 2016). With progression of the disease, tumor cells rupture the basal membrane of the epithelium, leading to growth of the primary tumor and its subsequent spread to distant tissues resulting in invasion and metastasis (Husain et al, 2016). Invasion and metastasis processes, in turn, include a sequence of events, such as migration of tumor cells to adjacent or distant sites, intravasation of these cells into the bloodstream, survival of tumor cells in the circulatory system, displacement and extravasation by the vascular wall towards the parenchyma, and formation of colonies and micro-metastases in the parenchyma, which may progress to metastatic lesions (Banyard and Bielenberg, 2015;Chapman et al, 2015;Pattabiraman and Weinberg, 2016;Brabletz et al, 2018).…”

“…In the process of tumor propagation, reactivation of the epithelial-mesenchymal transition (EMT) program is observed, leading to alterations in the expression of genes that code for transcription factors (Shibue and Weinberg, 2017), such as those of the SNAIL, TWIST and ZEB families (Brabletz et al, 2018). EMT involves increasing the invasion potential of tumor cells with decreased cell adhesion and increased ability for invasion and migration, as well as cellular morphological alterations, including tumor cell cytoskeletal rearrangements (Husain et al, 2016). In this reprogramming, there is a decrease in adhesion proteins, E-cadherins, and increased expression of Vimentin, 57 kDa protein encoded by a single copy of a gene, called VIM, located on the chromosome 10p13 (Yamashita et al, 2013;Figiel et al, 2017).…”

“…Studies have investigated the association of vimentin with some types of human cancers, such as prostate and breast cancers (Yamashita et al, 2013;Zhao et al, 2014;Du et al, 2018). Aberrant expression of vimentin and its association with metastatic potential in cervical cancer has been investigated by some authors Cheng et al, 2012;Yu et al, 2015;Husain et al 2016); however, there have been few such studies. We investigated a possible association between vimentin expression and clinical-pathological aspects and prognosis of cervical cancer.…”