AI Article Synopsis

  • The study investigates the role of SPOCK1, a protein linked to poor outcomes in various cancers, specifically focusing on its impact in ovarian cancer.
  • Both ovarian cancer cell lines used in the study showed increased DNA synthesis and cell migration when SPOCK1 was overexpressed, indicating its potential role in tumor progression.
  • High levels of SPOCK1 were found in the blood and tissues of ovarian cancer patients, and increased SPOCK1 expression correlated with shorter patient survival, suggesting it could be targeted for therapy and monitoring.

Article Abstract

Purpose: Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1) has been found in a variety of malignant tumors and is associated with a poor prognosis. We aimed to explore the role of SPOCK1 in ovarian cancer.

Methods: Ovarian cancer cell lines SKOV3 and SW626 were transfected with SPOCK1 overexpressing or empty vector using electroporation. Cells were studied by immunostaining and an automated Western blotting system. BrdU uptake and wound healing assays assessed cell proliferation and migration. SPOCK1 expression in human ovarian cancer tissues and in blood samples were studied by immunostaining and ELISA. Survival of patients with tumors exhibiting low and high SPOCK1 expression was analyzed using online tools.

Results: Both transfected cell lines synthesized different SPOCK1 variants; SKOV3 cells also secreted the proteoglycan. SPOCK1 overexpression stimulated DNA synthesis and cell migration involving p21. Ovarian cancer patients had increased SPOCK1 serum levels compared to healthy controls. Tumor cells of tissues also displayed abundant SPOCK1. Moreover, SPOCK1 levels were higher in untreated ovarian cancer serum and tissue samples and lower in recipients of chemotherapy. According to in silico analyses, high SPOCK1 expression was correlated with shorter survival.

Conclusion: Our findings suggest SPOCK1 may be a viable anti-tumor therapeutic target and could be used for monitoring ovarian cancer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10093273PMC
http://dx.doi.org/10.3390/cancers15072037DOI Listing

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