Year-end Sale % OFF 
Abstract
This study was performed to investigate the role of galectin-1 (Gal-1) in epithelial ovarian cancer (EOC) progression and chemoresistance. Tissue samples from patients with EOC were used to examine the correlation between Gal-1 expression and clinical stage of EOC. The role of Gal-1 in EOC progression and chemoresistance was evaluated in vitro by siRNA-mediated knockdown of Gal-1 or lentivirus-mediated overexpression of Gal-1 in EOC cell lines. To elucidate the molecular mechanisms underlying Gal-1-mediated tumor progression and chemoresistance, the expression and activities of some signaling molecules associated with Gal-1 were analyzed. We found overexpression of Gal-1 in advanced stages of EOC. Knockdown of endogenous Gal-1 in EOC cells resulted in the reduction in cell growth, migration, and invasion in vitro, which may be caused by Gal-1's interaction with H-Ras and activation of the Raf/extracellular signal-regulated kinase (ERK) pathway. Additionally, matrix metalloproteinase-9 (MMP-9) and c-Jun were downregulated in Gal-1-knockdown cells. Notably, Gal-1 overexpression could significantly decrease the sensitivities of EOC cells to cisplatin, which might be ascribed to Gal-1-induced activation of the H-Ras/Raf/ERK pathway and upregulation of p21 and Bcl-2. Taken together, the results suggest that Gal-1 contributes to both tumorigenesis and cisplatin resistance in EOC. Thus, Gal-1 is a potential therapeutic target for EOC.
Highlights
Cases are diagnosed at an advanced stage
We demonstrated that intracellular Gal-1 could promote Epithelial ovarian cancer (EOC) progression, chemoresistance to cisplatin, and increase H-Ras, p-Raf-1, p-extracellular signal-regulated kinase (ERK), matrix metalloproteinase-9 (MMP-9), c-Jun, p21, and Bcl-2 expression
Compared with normal ovarian tissues, Gal-1 was overexpressed in EOC tissues and tumor levels of Gal-1 were positively correlated with clinical stage, suggesting that Gal-1 participates in EOC progression
Summary
Cases are diagnosed at an advanced stage. High-grade serous EOC is frequently associated with intraperitoneal spread and distant metastases. After platinum-based chemotherapy, B25% of patients will develop resistance to the therapeutics within 6 months,[2] and the overall 5-year survival rate is B40%.3. Galectins are galactoside-binding glycoproteins with a conserved carbohydrate recognition domain.[4] Galectin-1 (Gal-1) is considered to be the prototypical galectins and is expressed in many tumor types such as astrocytoma, melanoma, and prostate, thyroid, colon, bladder, and ovarian cancers.[5,6] Increasing clinical evidence has confirmed that Gal-1 is involved in cancer progression and is associated with a poor prognosis in head and neck, prostate, lung, and ovarian cancers.[7,8,9,10,11] Gal-1 participates in tumor progression by evoking immunosuppression through the induction of activated T-cell apoptosis, transformation, angiogenesis, and metastasis.[12,13]. We found that Gal-1 was highly expressed in EOC tissues and its tumor levels were positively correlated with clinical stage. Gal-1 can promote the growth, migration, and invasion of EOC cells and their resistance to cisplatin. We revealed that Gal-1 could upregulate c-Jun, matrix metalloproteinase-9 (MMP-9), Bcl-2, and p21 expression, possibly through activation of the H-Ras/Raf/extracellular signal-regulated kinase (ERK) pathway
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
