Work

Integrin beta-like 1 overexpression stimulates invasiveness of ovarian cancer cells in vitro

Year: 2018

Type: article

Abstract: Background: In our previous microarray study we analyzed gene expression profile of over 100 ovarian cancer samples [1]. We identified two molecular subgroups of high grade serous ovarian cancers (HG-SOC) with distinct gene expression profiles and survival [2]. Among differentially expressed genes was an Integrin beta-like1 gene (ITGBL1). ITGBL1 is a poorly characterized protein, structurally cognate with integrin β. Our aim was to study whether and how ITGBL1 can influence the phenotype of ovarian cancer cells. Methods: ITGBL1 coding sequence was PCR-amplified from cDNA and cloned into pLNCX2 vector. Retroviral system was used to obtain two ovarian cancer cell lines: OAW42/ITGBL1(+) and SKOV3/ITGBL1(+) with overexpression of ITGBL1. Control cell lines were obtained by transduction with empty vector. A Matrigel cell invasion assay was performed using 24-well transwell inserts (coated with fibronectin and matrigel). Crystal violet staining of invaded cells was performed, then the dye was solubilized with 10% acetic acid and the absorbance was measured at a wavelength of 595 nm. Results: We compared invasion rate of control OAW42 and SKOV3 cells with that of isogenic cell lines containing ITGBL1 construct. The results indicate that ITGBL1 overexpression increases invasiveness of ovarian cancer cells. Conclusions: Our results indicate that ITGBL1 may increase ovarian cancer cell invasion rate. Along with our previous reported results that overexpression of ITGBL1 may increase migration, decrease adhesion [3] and has no effect on proliferation rate [4], these results suggests that ITGBL1 may play an important role in ovarian cancer progression enabling easier spreading of the cells within peritoneal cavity. [1]K.M.Lisowska, et al. (2014),Front.Oncol. DOI:10.3389/fonc.2014.00006. [2]K.M.Lisowska,et al.(2016),J.Cancer Res.Clin.Oncol.DOI:10.1007/s00432-016-2147-y. [3] A.J.Cortez, et al. (2016), Int. J. Gynecol. Cancer. Vol 26, sup. 3, p. 665 [4] A.J.Cortez, et al. (2017), Int. J. Gynecol. Cancer. Vol 27, sup. 4, p. 1931. Legal entity responsible for the study: Maria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch. Funding: Has not received any funding. Disclosure: All authors have declared no conflicts of interest.

Source: Annals of Oncology

DOI: 10.1093/annonc/mdy268.036

Authors: A.J. Cortez, K.A. Kujawa, P.A. Tudrej, K.M. Lisowska

Institution: The Maria Sklodowska-Curie National Research Institute of Oncology

Language: English

Topic: Cell Adhesion Molecules Research

Subfield: Immunology and Allergy

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $5,080