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.
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).
Cell viability, apoptosis, migration and invasion were determined using the Cell Counting Kit-8 (CCK-8) assay, flow cytometry and the Transwell assay, respectively.
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.
The effects of CXCR4, soluble VCAM1 and ADAM17 on NSCLC proliferation, migration and invasion were measured with CCK-8, monolayer scratch assay and transwell chamber, respectively.
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.
In the present study, the expression and function of miR‑767‑5p were examined in human glioblastoma multiforme (GBM) tissue specimens and cell lines. miR‑767‑5p expression levels were analyzed by quantitative reverse‑transcription PCR; cell proliferation was assessed by CCK‑8, colony formation and 5‑ethynyl‑2'‑deoxyuridine (EDU) assays; the cell cycle phase and apoptosis were detected by flow cytometry; and cell invasiveness was analyzed using wound healing and Transwell invasion 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.
Clone formation and CCK-8 assays were used to detect the proliferative capacity of the cells, and the transwell assay was used to explore their invasion and migration abilities.
The knockdown expression vectors of ANRIL were transfected into HepG2 cells, and qRT-PCR, CCK-8, flow cytometry, Transwell and western blot assays were performed to analyze the effect of ANRIL on cell proliferation, apoptosis, migration and invasion.
The effects of miR-99a on cell proliferation, migration and invasion were determined by Cell Counting Kit-8 (CCK-8) assay, transwell migration and invasion assay.
In the present study, a Cell Counting Kit-8 (CCK-8) assay was performed to observe proliferation in human gastric cancer cells (SGC-7901 and MGC-803 cells), and wound healing and Transwell chamber assays were performed to detect migration and invasion.
Colony formation and Cell Counting Kit-8 (CCK-8) assays were performed to measure cell proliferation ability and transwell analysis was used to detect cell invasion, and dual luciferase reporter assay was perform to analysis the interaction between the miR-423-5p and STMN1.