<i>Results:</i> The expression of miR-125a-5p in breast cancer cell lines, MDA-MB-157 cells, MDA-MB-361 cells and MDA-MB-415 cells, was significantly lower than that in normal breast epithelial cells, MCF-10A cells; The proliferation and invasion ability of MDA-MB-157 cells transfected with miR-125a-5p were significantly inhibited, and the apoptosis rate was significantly increased; Since GAB2 knocked down, the proliferation and invasion ability of MDA-MB-157 cells were significantly inhibited, while the apoptosis rate was significantly increased, the Bax protein expression was significantly down-regulated, and the Bcl-2 protein expression was significantly up-regulated; The dual-luciferase reporter assay demonstrated that miR-125a-5p can specifically target GAB2.
The expression of p53, p21, Bad, Bax, B‑cell lymphoma‑2 (Bcl‑2), cytochrome c (Cyt‑c), caspase‑3, Cox‑2, matrix metalloproteinase (MMP)‑2 and MMP‑9 was measured to further confirm the effects of CP‑31398 on cell migration, invasion and apoptosis.
Western blot was used for the determination of proteins and qPCR was for mRNA levels. miR-30a-5p expression was lowered in SCL-1 and A431 cells, and its upregulation suppressed EdU positive cells, colony numbers, migration, invasion and Bcl-2 expression, and elevated Bcl-2-associated X protein (Bax) and cleaved Caspase-3 expressions, arresting cell cycle in G1 phase.
In this study, we provided evidence that 17β-estradiol (E2) could significantly promote endometrial cancer cells viability, migration and invasion through activation of IL-6 pathway, which involved in its downstream pathway and target genes (p-Stat3, Bcl-2, Mcl-1, CyclinD1 and MMP2).
Alantolactone induced apoptosis of gastric cancer cells by regulating the expression of Bax, Bcl-2, and p53, which related to intrinsic apoptotic pathway, and suppressed colony formation, migration, and invasion by mediating the expression of matrix metalloproteinase (MMP)-2, MMP-7, and MMP-9.
RES, in a dose-dependent manner and in both cell lines, induced cell death and inhibited cell migration and invasion It also downregulated Bcl-2 levels, increased cleaved caspase-3, and GAL-3 protein (but not mRNA) levels, suggesting increased breakdown.
Finally, we showed miR-106a overexpression upregulated the levels of Bcl-2 and ABCG2, and downregulated the expression of P53, Bax, and RUNX3. miR-106a promotes breast cancer cell proliferation and invasion through upregulation of Bcl-2, ABCG2, and P53, and downregulation of Bax and RUNX3.
Restored miR-15b promoted Bax expression, apoptosis, and senescence, inhibited expression of LPAR3 and Bcl-2, the extent of PI3K and Akt phosphorylation, as well as ovarian cancer cell proliferation, migration, and invasion.
The overexpression of miR-98 or silencing of CLDN1 was shown to increase the expression of Bax and RUNX3 along with promoted cell apoptosis and arrested cells in G1 phase, while decreasing the expression of CLDN1, Bcl-2, C-myc, and PCNA with suppressed proliferation, migration, and invasion.
A miR‑92a‑3p mimic was found to promote ESCC cell proliferation and a miR‑92a‑3p inhibitor was found to reduce ESCC cell proliferation. miR‑92a‑3p mimic transfection accelerated ESCC cell migration and invasion and decreased ESCC cell apoptosis via the Bax/Bcl‑2 pathway and cleaved caspase‑3.
The expression of CyclinD1, apoptosis related proteins (p53, Bcl-2, Bax, pro-/Cleaved-Caspase-3), migration and invasion related proteins (MMP-9 and vimentin), and phosphatidylinositol 3'-kinase (PI3K)/protein kinase B (AKT) related proteins (p/t-PI3K, p/t-AKT) were examined by western blot.
Furthermore, disturbing the expression of Bcl‑2 partly reversed the changes to these proteins and also the pro‑proliferation, anti‑apoptosis and pro‑invasion potential of STC1.
The combination group induced more significant apoptosis and inhibition of migration and invasion by affecting proteins and mRNA of apoptosis, migration, and invasion related elements, such as Bcl-2, Bax, mTOR, and NF-?B.
Introduction of miR‑15a or knockdown of endogenous Bcl‑2 may reduce hypoxia-induced cell invasion and migration through the regulation of matrix metalloproteinases.
Compared to the blank and negative control groups, the miR-708 mimics and small-interfering RNA-bone morphogenetic protein and activin membrane-bound inhibitor groups exhibited decreases expressions of bone morphogenetic protein and activin membrane-bound inhibitor, Wnt10B, P53, and Bcl-2 and decreased proliferation, migration, and invasion capabilities, while increases in the apoptosis rate, expressions of vascular endothelial growth factor, Fas, Bax, Caspase-3, and cleaved Caspase-3; however, downregulated levels of TOPflash activity and β-catenin expression were recorded.
Immunodeficient nude mice were used to examine tumor growth following injection of MDA‑MB‑231 breast cancer cells. miR‑27a promoted proliferation in vitro and in vivo, and enhanced migration and invasion in TNBC cells. miR‑27a improved the survival of TNBC cells following irradiation. miR‑27a inhibited radiation‑induced apoptosis in TNBC cells by regulation of caspase 3/7 and Bcl‑2 expression.
Furthermore, miR-206 overexpression repressed cell proliferation, migration, and invasion in vitro, and the 3'-untranslated region (3'-UTR) of BAG3 was a direct target of miR-206. miR-206 overexpression also inhibited EGFR, Bcl-2, and MMP2/9 protein expression, but promoted Bax protein expression.
Overexpression of miR-423 enhanced the proliferation, and increased migration and invasion in endometrial cancer cells. miR-423 also decreased the sensitivity of endometrial cancer cells following cisplatin treatment. miR-423 inhibited cisplatin-induced apoptosis in endometrial cancer cells by regulation of caspase 3/7 and Bcl-2 expression.
In the present study, cell migration and invasion assays revealed that anti-apoptotic Bcl-2 protein induced migration and invasion without affecting cell proliferation in the BCap37 breast cancer cell line.
The present study investigated the expression of miR-21 in MGC803 gastric cancer cells and its effects on Bcl-2 expression and cell proliferation, apoptosis, and invasion.
Compared with the blank and NC groups, the miR-374 inhibitors + siRNA-Gadd45a group showed decreased miR-374 level; the siRNA-Gadd45a group showed elevated levels of P73, P16, Bax, caspase-3 and caspase-9, decreased levels of Gadd45a, P53, c-myc, and Bcl-2, reduced cell proliferation, migration, and invasion, and accelerated apoptosis. miR-374 induces apoptosis and inhibits proliferation, migration, and invasion of SCC cells through P53 signaling pathway by down-regulating Gadd45a.
Recombinant human S100A8 inhibited CRC cell migration and invasion, which was involved in epithelial-mesenchymal transition (E-cadherin and SNAIL) and apoptosis (BCL2).
Finally, the mRNA and protein levels of cell growth (PCNA and Cyclin E), apoptosis (Bcl-2 and Bax), invasion (matrix metalloproteinase-9) and epithelial-mesenchymal transition (EMT; Twist1 and E-cadherin) related moderators were affected by SOX12 knockdown.