Abstract
BackgroundColorectal cancer (CRC) exhibits high risks of morbidity and mortality.ObjectiveTo investigate the effect of scavenger receptor class A member 5 (SCRAR5) on CRC and its mechanism on modulation of cancer development.MethodsThe SCRAR5 expression in four kinds of CRC cell lines (SW620, SW480, HT29, and HCT116) was measured by quantitative PCR and western blotting, respectively. The effects of SCRAR5 abnormal expression on cell proliferation, apoptosis, and migration were analyzed by CCK-8 assay, EdU assay, colony-forming assay, flow cytometry assay, Transwell assay and wound healing assay, respectively. Meanwhile, the involvements of PI3K/AKT/mTOR pathway with the role of SCRAR5 were investigated by western blotting. Afterwards, the in vivo effects of SCRAR5 abnormal expression on CRC xenograft mice were finally investigated by evaluating tumor volume, apoptosis and Ki67 expression.ResultsSCRAR5 was lowly expressed in CRC cell lines, especially SW480 cells. Up-regulation of SCRAR5 significantly promoted cell apoptosis, reduced cell proliferation and migration in SW480 cells. Notably, SCRAR5 overexpression obviously inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Reversely, SCRAR5 silence exhibited promoting effects on HT29 cells. Consistently, in vivo experiments also revealed that SCRAR5 overexpression remarkably suppressed tumor volume and Ki67 expression, as well as promoted cell apoptosis.ConclusionsOverall, up-regulating of SCRAR5 obviously inhibited CRC tumor growth in vitro and in vivo, which might be related to PI3K/AKT/mTOR pathway.
Highlights
As the common digestive system malignant tumors, and colorectal cancer (CRC) exhibits high risks of morbidity and mortality (Keum and Giovannucci 2019; Siegel et al 2020)
Cell proliferation assays revealed that compared with control and OE-NC or siNC groups, scavenger receptor class A member 5 (SCRAR5) overexpression obviously inhibited cell viability in time-dependent manner (p < 0.05, Fig. 2B), decreased the ethynyl-2′- deoxyuridine (EdU) fluorescence (Fig. 2C), and reduced the clone number (Fig. 2D); reversely, SCRAR5 knockdown increased cell viability (Fig. 2B), the EdU fluorescence (Fig. 2C), and the clone number (Fig. 2D)
SCRAR5 overexpression induced cell apoptosis, while SCRAR5 knockdown suppressed cell apoptosis when compared with control cells (Fig. 2E)
Summary
As the common digestive system malignant tumors, and colorectal cancer (CRC) exhibits high risks of morbidity and mortality (Keum and Giovannucci 2019; Siegel et al 2020). Over the last few decades, increasing researchers investigate the prognosis biomarkers in order to search for the effective treatment methods for cancers (Shukla 2017). Objective To investigate the effect of scavenger receptor class A member 5 (SCRAR5) on CRC and its mechanism on modulation of cancer development. The involvements of PI3K/AKT/mTOR pathway with the role of SCRAR5 were investigated by western blotting. Afterwards, the in vivo effects of SCRAR5 abnormal expression on CRC xenograft mice were investigated by evaluating tumor volume, apoptosis and Ki67 expression. In vivo experiments revealed that SCRAR5 overexpression remarkably suppressed tumor volume and Ki67 expression, as well as promoted cell apoptosis. Conclusions Overall, up-regulating of SCRAR5 obviously inhibited CRC tumor growth in vitro and in vivo, which might be related to PI3K/AKT/mTOR pathway
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