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Research Paper Volume 13, Issue 22 pp 24850-24865
Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells
Relevance score: 7.336737Jiajia Zhang, Ping Wang, Yanli Cui
Keywords: laryngocarcinoma, long noncoding RNA nuclear paraspeckle assembly transcript 1, miR-524-5p, histone deacetylationase 1, phosphatase and tensin homolog /protein kinase B signaling pathway
Published in Aging on November 27, 2021
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Research Paper Volume 11, Issue 18 pp 7492-7509
PTEN loss regulates alveolar epithelial cell senescence in pulmonary fibrosis depending on Akt activation
Relevance score: 9.2622Ting Qiu, Yaqiong Tian, Yujuan Gao, Miao Ma, Hui Li, Xiaoqin Liu, Hongyan Wu, Yingwei Zhang, Hui Ding, Mengshu Cao, Ji Zhang, Jinghong Dai, Jingyu Chen, Hourong Cai
Keywords: aging, cellular senescence, pulmonary fibrosis, phosphatase and tension homolog deleted on chromosome ten, protein kinase B
Published in Aging on September 17, 2019
Aging-related markers are significantly overexpressed in the lung tissues of IPF patients. Human lung tissues of IPF (n = 12) and age-matched normal lung tissues (n = 12) were analyzed. (A) Representative images of HE staining of lung tissues (original magnification, 100×). (B) Representative images of the aging-related marker, P21WAF1, via IHC staining of lung tissues (original magnification, 100× in control and 200× in IPF). (C) Representative results of SA-β-Gal staining of lung tissues (original magnification, 100×). (D) Enlarged images of SA-β-Gal staining (200×). (E) Immunofluorescence staining of SP-C (an AEC2-specific marker, red) and P21WAF1(green) was conducted to confirm senescent marker expression in AECs (original magnification, 400×). (F, G) P21WAF1 senescent marker in lung tissues was measured by western blotting. Each dot represents an individual lung tissue. **p < 0.01. Unpaired, two-tailed Student’s t test.
Loss of PTEN and activation of the AKT pathway in lung tissue from IPF patients. (A) Representative results of IHC staining for PTEN and p-AKT 473 in lung tissues (original magnification, 200× for PTEN and 100× for p-AKT 473). (B) Immunofluorescence staining for both SP-C (red) and PTEN (green) were conducted to examine the spatial distribution of PTEN (original magnification, 200×). (C–E) Western blot analysis was applied to detect the expression of PTEN and activation of the AKT pathway. Each dot represents an individual lung tissue. **p < 0.01. Unpaired, two-tailed Student’s t test.
Decrease of PTEN and activation of the AKT pathway in the senescent cell model. Gradually increasing concentrations of bleomycin was added to culture medium to stimulate A549 cells for 72 hours followed by transfer to fresh FBS-free medium for another 24 hours. (A, B) SA-β-Gal staining was performed to detect cellular senescence (original magnification, 200×). (C, D) The expression of the aging-related marker, P21WAF1, was detected by western blot analysis. (E–G) PTEN loss and AKT pathway activation were observed. Data are shown as the mean ± SEM, n ≥ 3 per group. *p < 0.05, ***p < 0.001. One-way ANOVA followed by Dunnett’s Multiple Comparison Test.
Change of PTEN expression affects cell senescence through AKT pathway activation. Genetic overexpression of PTEN in A549 cells was achieved by a transduction of a lentiviral vector followed by bleomycin (10 μg/ml) stimulation for 72 hours and transfer to fresh medium for 24 hours. (A, B) Cellular senescence was detected by SA-β-Gal staining (original magnification, 200×). (C–G) Western blot analysis was performed to confirm alteration of P21WAF1 and targets of the PTEN/AKT pathway. Lentiviral vector was used to knockdown PTEN expression in A549 cells. Bleomycin was then added to the culture medium to stimulate cells for 72 hours followed by transfer to fresh FBS-free medium for another 24 hours. (H, I) SA-β-Gal staining was applied to detect cellular senescence (original magnification, 200×). (J–N) Change of P21WAF1 and expression of PTEN/AKT targets were determined by western blotting. Data are shown as the mean ± SEM, n ≥ 3 per group. *p < 0.05, **p < 0.01, ***p < 0.001. One-way ANOVA followed by Dunnett’s Multiple Comparison Test.
Knockdown AKT2, but not AKT1, rescues cell from bleomycin-induced cell senescence. The expression of AKT2 or AKT1 was knocked down by lentiviral vector in A549 cells followed by bleomycin (10 μg/ml) stimulation for 72 hours and transfer to fresh medium for 24 hours. (A, B) Cellular senescence was detected by SA-β-Gal staining (original magnification, 200×). (C–E) Western blotting was performed to confirm the change of P21WAF1, PTEN and AKT2. (F–G) Cellular senescence after AKT1 knockdown was analyzed by SA-β-Gal staining (original magnification, 200×). (H, I). Expression of P21WAF1 and AKT1 was confirmed by western blotting. Data are shown as the mean ± SEM, n ≥ 3 per group. *p < 0.05, **p < 0.01, ***p < 0.001. One-way ANOVA followed by Dunnett’s Multiple Comparison Test.
Inhibition of Akt activation attenuates AEC senescence. Inhibitor (20 μm/L LY294002 or 5 μg/ml MK2206) of the AKT pathway was added 1 hour before bleomycin (10 μg/ml). After 72 hours, the medium was changed to fresh medium for 24 hours. AKT inactivation and P21WAF1 expression induced by LY294002 (A–C) or MK2206 (F–H) were detected by western blotting. Cellular senescence after inhibitor LY294002 (D, E) or MK2206 (I, J) pretreatment was analyzed by SA-β-Gal staining. Data are shown as the mean ± SEM, n ≥ 3 per group. *p < 0.05. One-way ANOVA followed by Dunnett’s Multiple Comparison Test.
Akt inactivation rescues AEC senescence in vitro. After PTEN was stably knocked down, an inhibitor of the AKT pathway (20 μm/L LY294002 or 5 μg/ml MK2206) was added 1 hour before bleomycin (10 μg/ml) to A549 cells for 72 hours followed by a fresh medium transfer for 24 hours. (A, B) Rescue of cell senescence by LY294002 was determined by SA-β-Gal staining (original magnification, 200×), and decreased expression of P21WAF1 (C, D) was confirmed by western blot. Rescue of cell senescence by MK2206 was determined by SA-β-Gal staining (E, F) and P21WAF1 expression (G, H). Data are shown as the mean ± SEM, n ≥ 3 per group. *p < 0.05, **p < 0.01. One-way ANOVA followed by Dunnett’s Multiple Comparison Test.
Akt inactivation attenuates AEC senescence and pulmonary fibrosis in vivo. C57BL/6 male mice were randomly divided into vehicle group (n = 6), bleomycin group (n = 6) and inhibitor group (n=6). Mice in the vehicle group were intratracheally injected with 50 μl of 0.9% saline, and mice in the bleomycin group and inhibitor group were injected intratracheally with 50 μl of 5 mg/kg bleomycin. From the day of bleomycin injection, mice in the inhibitor group were treated daily with LY294002 (50 mg/kg) through intraperitoneal injection. On day 14 after bleomycin or saline treatment, lungs were harvested. (A, B) Expression of the P21WAF1 senescent marker and the collagen1α fibrotic marker was detected by western blot analysis. Dots in the graph represent values for each individual mouse. *p < 0.05, ***p < 0.001. One-way ANOVA followed by Dunnett’s Multiple Comparison Test. (C) Representative results of HE and Masson staining of mouse lung tissues.
PTEN physically associates with Akt. In A549 cells, immunoprecipitation of PTEN resulted in the co-IP of AKT, and immunoprecipitation of AKT also resulted in the co-IP of PTEN.