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Decreased expression of miR-132 in CRC tissues and its inhibitory function on tumor progression
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AbstractObjectives Colorectal cancer (CRC) is among the most common types of malignancies in the worldwide, and microRNAs (miRNAs) emerge as key regulators in carcinogenesis and tumor progression. Here we intended to address the expression and function of miR-132 in CRC cells. Methods Paired CRC tissues and several established cell lines were firstly collected. We performed qPCR to detect the expression of miR-132 in these tissues and cell lines. Cell proliferation and apoptosis were respectively monitored by CCK-8 assay and Annexin-V/PI staining followed by flow cytometry, after miR-132 was transiently overexpressed in RKO cells. Afterwards, Luciferase reporter assays were performed to examine the targeting of YAP1 by miR-132. Finally, qPCR and western blotting were also carried out to validate this targeting. Results MiR-132 was significantly decreased in CRC and its overexpression in RKO cells exerted tumor suppressing effects, including cell growth arrest and apoptosis promotion. Additionally, we proved that miR-132 could negatively regulate the expression of YAP1. Conclusion Our findings suggested that miR-132 was downregulated in CRC, and played as a tumor suppressor to inhibit cell proliferation and induce apoptosis. And these anti-tumor activities might be related with the targeting of YAP1 by miR-132.
Title: Decreased expression of miR-132 in CRC tissues and its inhibitory function on tumor progression
Description:
AbstractObjectives Colorectal cancer (CRC) is among the most common types of malignancies in the worldwide, and microRNAs (miRNAs) emerge as key regulators in carcinogenesis and tumor progression.
Here we intended to address the expression and function of miR-132 in CRC cells.
Methods Paired CRC tissues and several established cell lines were firstly collected.
We performed qPCR to detect the expression of miR-132 in these tissues and cell lines.
Cell proliferation and apoptosis were respectively monitored by CCK-8 assay and Annexin-V/PI staining followed by flow cytometry, after miR-132 was transiently overexpressed in RKO cells.
Afterwards, Luciferase reporter assays were performed to examine the targeting of YAP1 by miR-132.
Finally, qPCR and western blotting were also carried out to validate this targeting.
Results MiR-132 was significantly decreased in CRC and its overexpression in RKO cells exerted tumor suppressing effects, including cell growth arrest and apoptosis promotion.
Additionally, we proved that miR-132 could negatively regulate the expression of YAP1.
Conclusion Our findings suggested that miR-132 was downregulated in CRC, and played as a tumor suppressor to inhibit cell proliferation and induce apoptosis.
And these anti-tumor activities might be related with the targeting of YAP1 by miR-132.
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