Abstract 767
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.
Clinical trial identification
Legal entity responsible for the study
Maria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch.
Funding
Has not received any funding.
Editorial Acknowledgement
Disclosure
All authors have declared no conflicts of interest.
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