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PIN inhibits TGF-β1-induced EMT in A549 and <t>Beas2B</t> cells. (A) PIN possesses a stilbene structure. (B) The effect of various concentrations of PIN on cell viability after 48 h of incubation with 5 ng/mL TGF-β1 in A549 and Beas2B cells (n = 4). (C,D) The impact of a gradient of PIN concentrations on the mRNA expression levels of E-cadherin and Vimentin in TGF-β1-induced A549 and Beas2B cells. (E–G) Changes in E-cadherin and Vimentin protein expression levels in TGF-β1-induced A549 and Beas2B cells with varying concentrations of PIN intervention. n = 3; compared with the control group, ## P < 0.01, and # P < 0.05; compared with the model group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference. Error bars represent the mean ± standard deviation.
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TMEM147 promotes the proliferation, migration and invasion of LUAD in vitro (A) The protein expression levels of TMEM147 in BEAS2B, HCC827, NCI–H1975, NCI–H1299, A549 and PC9 cell lines were detected. (B) Western blot analysis of TMEM147 expression in NCI–H1299 and A549 cells (siTMEM147-1,siTMEM147-2 and control). (C–D) NCI–H1299 and A549 cells were used to determine clone formation assays. (E–G) Transwell assays showing migration and invasion abilities. (H–I) Wound-healing assays. Scale bars: Scale bars: 100 μm (100 × ), 50 μm (200 × ).∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, NS, no significance.

Journal: Biochemistry and Biophysics Reports

Article Title: Integrated multi-omics analysis reveals TMEM147 as an immunosuppressive prognostic biomarker in LUAD

doi: 10.1016/j.bbrep.2025.102281

Figure Lengend Snippet: TMEM147 promotes the proliferation, migration and invasion of LUAD in vitro (A) The protein expression levels of TMEM147 in BEAS2B, HCC827, NCI–H1975, NCI–H1299, A549 and PC9 cell lines were detected. (B) Western blot analysis of TMEM147 expression in NCI–H1299 and A549 cells (siTMEM147-1,siTMEM147-2 and control). (C–D) NCI–H1299 and A549 cells were used to determine clone formation assays. (E–G) Transwell assays showing migration and invasion abilities. (H–I) Wound-healing assays. Scale bars: Scale bars: 100 μm (100 × ), 50 μm (200 × ).∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, NS, no significance.

Article Snippet: The human lung epithelial cell line BEAS2B and four LUAD-derived cell lines (A549, NCI–H1299, HCC827 and NCI–H1975) were acquired from ATCC.

Techniques: Migration, In Vitro, Expressing, Western Blot, Control

PIN inhibits TGF-β1-induced EMT in A549 and Beas2B cells. (A) PIN possesses a stilbene structure. (B) The effect of various concentrations of PIN on cell viability after 48 h of incubation with 5 ng/mL TGF-β1 in A549 and Beas2B cells (n = 4). (C,D) The impact of a gradient of PIN concentrations on the mRNA expression levels of E-cadherin and Vimentin in TGF-β1-induced A549 and Beas2B cells. (E–G) Changes in E-cadherin and Vimentin protein expression levels in TGF-β1-induced A549 and Beas2B cells with varying concentrations of PIN intervention. n = 3; compared with the control group, ## P < 0.01, and # P < 0.05; compared with the model group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference. Error bars represent the mean ± standard deviation.

Journal: Frontiers in Pharmacology

Article Title: Pinostilbene inhibits lung epithelial-mesenchymal transition and delays pulmonary fibrosis by modulating the PI3K/Akt pathway

doi: 10.3389/fphar.2025.1614546

Figure Lengend Snippet: PIN inhibits TGF-β1-induced EMT in A549 and Beas2B cells. (A) PIN possesses a stilbene structure. (B) The effect of various concentrations of PIN on cell viability after 48 h of incubation with 5 ng/mL TGF-β1 in A549 and Beas2B cells (n = 4). (C,D) The impact of a gradient of PIN concentrations on the mRNA expression levels of E-cadherin and Vimentin in TGF-β1-induced A549 and Beas2B cells. (E–G) Changes in E-cadherin and Vimentin protein expression levels in TGF-β1-induced A549 and Beas2B cells with varying concentrations of PIN intervention. n = 3; compared with the control group, ## P < 0.01, and # P < 0.05; compared with the model group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference. Error bars represent the mean ± standard deviation.

Article Snippet: A549 and Beas2B cells (Procell, Wuhan, China) were cultured in an incubator at 37 °C in 5% CO 2 with RPMI-1640 (Gibco, Sigma Aldrich, Søborg, Denmark) containing 10% foetal bovine serum (Gibco, Sigma Aldrich, Denmark) and 1% penicillin-streptomycin (Gibco, Sigma Aldrich, Denmark).

Techniques: Incubation, Expressing, Control, Standard Deviation

Adhesion and scratch assays of TGF-β1-induced A549 and Beas2B cells treated with 5 μM PIN. (A) Representative stained adhesion images of A549 and Beas2B cells after 48 h. (B) Adhesion of A549 and Beas2B cells after 48 h. (C) Migration of A549 and Beas2B cells after 48 h. (D) Migration of A549 and Beas2B cells after 48 h. Mean ± standard deviation; n = 3; compared to the control group, ## P < 0.01; compared to the model group, ** P < 0.01. Magnification: 100 times.

Journal: Frontiers in Pharmacology

Article Title: Pinostilbene inhibits lung epithelial-mesenchymal transition and delays pulmonary fibrosis by modulating the PI3K/Akt pathway

doi: 10.3389/fphar.2025.1614546

Figure Lengend Snippet: Adhesion and scratch assays of TGF-β1-induced A549 and Beas2B cells treated with 5 μM PIN. (A) Representative stained adhesion images of A549 and Beas2B cells after 48 h. (B) Adhesion of A549 and Beas2B cells after 48 h. (C) Migration of A549 and Beas2B cells after 48 h. (D) Migration of A549 and Beas2B cells after 48 h. Mean ± standard deviation; n = 3; compared to the control group, ## P < 0.01; compared to the model group, ** P < 0.01. Magnification: 100 times.

Article Snippet: A549 and Beas2B cells (Procell, Wuhan, China) were cultured in an incubator at 37 °C in 5% CO 2 with RPMI-1640 (Gibco, Sigma Aldrich, Søborg, Denmark) containing 10% foetal bovine serum (Gibco, Sigma Aldrich, Denmark) and 1% penicillin-streptomycin (Gibco, Sigma Aldrich, Denmark).

Techniques: Staining, Migration, Standard Deviation, Control

Inhibition of PI3K/Akt signaling pathway activation in A549 and Beas2B cells by PIN. (A–C) A549 and Beas2B cells were treated with TGF-β1 (5 ng/mL) in the presence of varying concentrations of PIN (1, 2.5, and 5 μM) for a duration of 48 h. Subsequently, cell lysates were harvested and subjected to western blot analysis to evaluate the expression levels of PI3K, p-PI3K, Akt, and p-Akt. Mean ± standard deviation; n = 3; compared to the control group, ## P < 0.01, and # P < 0.05; compared to the model group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference. (D–F) Examination of the Impact of SC79 and LY294002 on the PI3K/Akt Pathway in A549 and Beas2B Cells. Cells were exposed to SC79 (20 μM) and LY294002 (10 μM) along with 5 μM PIN for a period of 48 h. Following this treatment, cell lysates were obtained and analyzed for the expression of PI3K, p-PI3K, Akt, and p-Akt using western blotting techniques. Mean ± standard deviation; n = 3; compared to the control group, ## P < 0.01, and # P < 0.05; compared to the SC79 group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference.

Journal: Frontiers in Pharmacology

Article Title: Pinostilbene inhibits lung epithelial-mesenchymal transition and delays pulmonary fibrosis by modulating the PI3K/Akt pathway

doi: 10.3389/fphar.2025.1614546

Figure Lengend Snippet: Inhibition of PI3K/Akt signaling pathway activation in A549 and Beas2B cells by PIN. (A–C) A549 and Beas2B cells were treated with TGF-β1 (5 ng/mL) in the presence of varying concentrations of PIN (1, 2.5, and 5 μM) for a duration of 48 h. Subsequently, cell lysates were harvested and subjected to western blot analysis to evaluate the expression levels of PI3K, p-PI3K, Akt, and p-Akt. Mean ± standard deviation; n = 3; compared to the control group, ## P < 0.01, and # P < 0.05; compared to the model group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference. (D–F) Examination of the Impact of SC79 and LY294002 on the PI3K/Akt Pathway in A549 and Beas2B Cells. Cells were exposed to SC79 (20 μM) and LY294002 (10 μM) along with 5 μM PIN for a period of 48 h. Following this treatment, cell lysates were obtained and analyzed for the expression of PI3K, p-PI3K, Akt, and p-Akt using western blotting techniques. Mean ± standard deviation; n = 3; compared to the control group, ## P < 0.01, and # P < 0.05; compared to the SC79 group, ** P < 0.01, and * P < 0.05; ns indicates no statistically significant difference.

Article Snippet: A549 and Beas2B cells (Procell, Wuhan, China) were cultured in an incubator at 37 °C in 5% CO 2 with RPMI-1640 (Gibco, Sigma Aldrich, Søborg, Denmark) containing 10% foetal bovine serum (Gibco, Sigma Aldrich, Denmark) and 1% penicillin-streptomycin (Gibco, Sigma Aldrich, Denmark).

Techniques: Inhibition, Activation Assay, Western Blot, Expressing, Standard Deviation, Control