cellular proliferation  (MedChemExpress)

Journal: FASEB BioAdvances

Article Title: MicroRNA 15a and 16 Regulate Proteostasis in Non‐Small Cell Lung Cancer

doi: 10.1096/fba.2026-00075

Figure Lengend Snippet: MiR15a/16 suppress cellular growth and protein anabolism in NSCLC. Overexpression of miR15a/16 in LUSC (H446) and LUAD (A549) cells slows cellular proliferation over 72 h (panel A, B) and blunts protein synthesis rates (panel C, D) in models of NSCLC. For proliferation experiments (panels A, B) n = 5, for protein synthesis measurements n = 4. * indicates a difference of p < 0.05, **** indicates a difference of p < 0.0001.

Article Snippet: We measured cellular proliferation using a WST‐8 assay (HY‐K0301; MedChemExpress, Monmouth Junction, NJ, USA), a colorimetric assay that produces a tetrazolium salt in proportion to the number of cells in a sample well.

Techniques: Over Expression

Journal: Cell Death & Disease

Article Title: The TRIM3/TLR3 axis overrides IFN-β feedback inhibition to suppress NSCLC progression

doi: 10.1038/s41419-025-08265-w

Figure Lengend Snippet: A – F CCK-8 and colony formation assays were performed to validate the effect of the TRIM3/TLR3 axis on A549, H1299 and LLC cell proliferation following 10 ng/mL poly(I:C) stimulation (n = 4). Statistical significance was analyzed using one-way ANOVA. G Schematic diagram depicting the experimental workflow of the in vivo experiments. H – J Syngeneic mouse models were established to evaluate the effect of the TRIM3/TLR3 axis on tumor growth, with intraperitoneal poly(I:C) (1 mg/kg) injections administered every 3 days. Representative images ( H ) and tumor weights ( I ) and volumes ( J ) are shown (n = 8). Statistical significance was analyzed using one-way ANOVA. K IHC analysis was performed to evaluate IFN-β, CD4, CD49b, CD86, and CD163 expression in mouse tumors. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: Cellular proliferation was assessed using a cell counting kit-8 (CK04, Dojindo, Kumamoto, Japan) according to the manufacturer’s protocol.

Techniques: CCK-8 Assay, In Vivo, Expressing

Journal: BMC Gastroenterology

Article Title: Elucidating the role of AC026412.3 in hepatocellular carcinoma: a prognostic disulfidptosis-related LncRNAs model perspective

doi: 10.1186/s12876-025-04174-6

Figure Lengend Snippet: Functional experiments aginst AC026412.3 in HCC cells. A Expression levels of AC026412.3 in paired clinical samples of HCC and paracancerous tissues. Upon paired analysis, the expression of AC026412.3 is significantly elevated in HCC tissues as compared to the corresponding paracancerous normal tissues. B Expression levels of AC026412.3 in HCC cell lines HepG2, Hep3B2.1-7, HCC-LM3, and normal liver tissue LO2. AC026412.3 was expressed at higher levels in all tested HCC cell lines relative to the LO2 cells. C Relative extression of AC026412.3 after transfection with siRNAs. After RNA interference, the expression levels of the AC026412.3 were significantly reduced. D The Cell Counting Kit-8 (CCK-8) assay revealed a marked reduction in proliferation following siRNA-mediated knockdown of AC026412.3 . E The colony formation assay demonstrated a reduction in proliferative capacity following the disruption of AC026412.3 . F The knockdown of AC026412.3 led to a statistically significant decrease in the wound healing rate of HCC cells. G Transwell assays demonstrated a notable decline in cell invasion and migration capabilities post-knockdown. Significant differences are indicated by * P < 0.05 and ** P < 0.01

Article Snippet: Cellular proliferation was evaluated using the Cell Counting Kit-8 (CCK-8, Beyotime Biotechnology, China).

Techniques: Functional Assay, Expressing, Transfection, Cell Counting, CCK-8 Assay, Knockdown, Colony Assay, Disruption, Migration

Journal: BMC Gastroenterology

Article Title: Elucidating the role of AC026412.3 in hepatocellular carcinoma: a prognostic disulfidptosis-related LncRNAs model perspective

doi: 10.1186/s12876-025-04174-6

Figure Lengend Snippet: The Impact of LncRNA AC026412.3 on lung metastasis and related molecular markers in a mouse model. A Comparative analysis of tumour cell infiltration in lung tissues of nude mice following tail vein injection of HCC cells transfected with either control vector (pL-NC- AC026412.3 ) or AC026412.3 -knockdown vector (pL-sh- AC026412.3 -LM3). H&E staining was employed to assess the extent of colonization. The results demonstrate a marked reduction in tumour cell infiltration in the pL-sh- AC026412.3 -LM3 group compared to controls, highlighting the role of AC026412.3 in promoting tumour growth, invasion, and metastasis. B Immunohistochemical analysis of key markers associated with tumour invasion and proliferation, including MMP9, E-cadherin, Vimentin, and Ki-67, in lung tissues from mice injected with pL-NC-LM3 or pL-sh- AC026412.3 -LM3 cells. The IHC data reveal an upregulation of E-cadherin and a downregulation of Ki-67, Vimentin, and MMP9 in the pL-sh- AC026412.3 group, corroborating the hypothesis that knockdown of AC026412.3 attenuates cell proliferation and metastasis. Significant differences are indicated (** P < 0.01; two-tailed Student’s t-test)

Article Snippet: Cellular proliferation was evaluated using the Cell Counting Kit-8 (CCK-8, Beyotime Biotechnology, China).

Techniques: Injection, Transfection, Control, Plasmid Preparation, Knockdown, Staining, Immunohistochemical staining, Two Tailed Test