The present study assessed expression, functions and mechanisms of miR‑20a‑5p in the regulation of HNSCC cell proliferation, migration and invasion. miR‑20a‑5p expression in HNSCC cell lines and tissues was detected using qRT‑PCR, while miR‑20a‑5p mimics and inhibitor were transfected into HNSCC cells for assessment of the effects using different assays (CCK‑8, wound healing and Transwell assays) and expression of miR‑20a‑5p‑targeting genes (using western blot and luciferase reporter assays).
CMTM8 was successfully overexpressed by lentivirus in EJ and T24 cells, and the CCK‑8 and Transwell assays showed that CMTM8 overexpression decreased cell proliferation, migration and invasion in vitro.
CCK-8, colony formation, and Matrigel invasion assays demonstrated that the overexpression of Eya2 promoted proliferation, colony number, and invasion while Eya2 shRNA inhibited proliferation rate, colony formation, and invasion ability.
The qRT-PCR and western blot were performed to measure RPL34 expression, CCK-8 and flow cytometry to observe cell growth and apoptosis, and wound healing and transwell to detect cell migration and invasion.
By using cell counting kit-8 (CCK-8) assays, colony formation assays, flow cytometric analyses and Transwell assays, our data suggested that up-regulation of miR-92a promoted the proliferation, migration, and invasion of MNNG and U2OS cells, while inhibiting their apoptosis.
Flow cytometry analysis, CCK-8 assay, and Transwell assay were applied to detect the effects of TFAP2A-AS1 overexpression on cell cycle, apoptosis, viability, and invasion of BC cells.
The biological functions of miR-127-3p and ITGA6 in OS were investigated by following experiments: cell counting kit 8 (CCK-8) and colony formation assays to inspect cell proliferation, flow cytometry, and caspase 3 activity assay to examine apoptosis, and transwell and wound healing assays to analyze invasion and migration.
In vitro functional assays (CCK-8 assay, colony formation assay, and cell invasion assay) revealed that knock-down of TUG1 by small RNA inference significantly inhibited cell proliferation, colony formation and cell invasion in ovarian cancer cells.
RNA interference (RNAi) or pEABE-bleo IGF-1R plasmid were used for silencing or overexpressing IGF-1R, Western blot (WB) analysis was used for IGF-1R expression, CCK-8 for proliferation, and transwell assay for migration and invasion.
Following treatment of the cells with 2, 4 and 8 µM ATO for 48 h, cell counting kit‑8 (CCK‑8), Transwell and western blot assays were used to determine the extent of human MHCC97‑H HCC cell proliferation, apoptosis, invasion and B7‑H4 expression, respectively.
Subsequently, a validation with Real-time RT-PCR was performed to analyze the miR-22 expression level, and a CCK-8 proliferation assay and transwell migration and invasion assays were carried out.
In vitro functional studies of CCK-8 demonstrated that silencing ALDOB expression significantly (P<0.05) inhibited proliferation, migration and invasion of colon cancer cells.
Western blot, CCK-8 method, Transwell and flow cytometry were used to detect protein expression, cell proliferation, cell migration and invasion as well as cell apoptosis, respectively.
CCK-8 and clone formation experiments also revealed that interference on ASAP1-IT1 expression could inhibit the proliferation of NSCLC cells, while the transwell experiment showed that the interference on ASAP1-IT1 expression could block the migration and invasion ability of NSCLC cells.
CCK-8 assay, MTT assay, colony formation assay, and cell invasion assay results showed that knock-down of TUG1 by siRNA transfection suppressed cell growth, cell proliferation, and cell invasion in OSCC cell lines (Tca8113 and TSCCA).
Quantitative real-time PCR (qRT-PCR) was performed to determine relevant gene expression levels; western blot was performed to determine protein expression levels; CCK-8, colony formation, wound healing and Transwell invasion assays were used to determined CRC cell proliferation, migration and invasion; in vivo tumor growth was assessed in xenograft mice model.
Cell Counting Kit-8 (CCK-8), flow cytometry, the scratch test, Transwell migration assay and Boyden chamber assays were used to detect cell proliferation, apoptosis, migration and invasion.
To assess the function of miR‑195‑3p in RCC cell lines, cell proliferation was examined using MTT and CCK‑8 assays, mobility was assessed using a cell scratch assay, Transwell migration assay and invasion assay, and apoptosis was examined using flow cytometry.
In A549 and H1299 cells, upregulation of ARHGAP6 inhibited tumor growth and metastasis and reduced the levels of MMP9, VEGF and p‑STAT3, while the levels STAT3 were unchanged, as demonstrated by CCK‑8, migration and invasion assays as well as western blot analysis.