The overexpression of metastasis‑associated in
colon cancer 1 (MACC1) has been demonstrated not only in
colon cancer, but also in various other types of
cancer.
Gliomas are the most common type of intracranial
tumors, and recent studies have reported MACC1 to be involved in human
glioma progression. The present study aimed to investigate the effects of MACC1 expression silencing in
glioma cells using RNA interference, in order to determine the underlying biological mechanisms of
glioma progression, including proliferation, apoptosis, invasion and
metastasis. The expression levels of MACC1 were determined in various types of U251
glioma cells using western blot analyses. MACC1‑specific
short hairpin RNA (
shRNA) was used to silence the expression of MACC1 in the U251 cells. The results obtained following MACC1 silencing demonstrated a significant inhibition of cell proliferation, invasion and migration, as well as a marked enhancement of apoptosis. MACC1 shRNA‑induced inhibition of cell proliferation was observed by colony forming and MTT assays, and cell apoptosis was measured using flow cytometry and Hoechst staining. In addition, inhibition of cell invasion and migration was assessed using wound healing and transwell assays. Western blotting and fluorescence‑activated cell sorting (FACS) revealed a G0/G1 phase cell cycle arrest regulated by
cyclins D1 and E; cell apoptosis regulated by caspase‑3; and cell invasion and migration regulated by
matrix metalloproteinases 2 and 9, respectively. The present study demonstrated that the expression levels of MACC1 were significantly correlated with the biological processes underlying
glioma cell proliferation, invasion and
metastasis. Therefore, MACC1 may serve as a promising novel therapeutic target in human
glioma. Notably, the inhibition of MACC1 expression by
shRNA may prove to be an effective genetic therapeutic strategy for
glioma treatment.