scholarly journals Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway

2019 ◽  
Vol Volume 11 ◽  
pp. 7909-7923 ◽  
Author(s):  
Cong Zhang ◽  
Xiangping Chang ◽  
Dongshan Chen ◽  
Feilong Yang ◽  
Zeyan Li ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Bladder Cancer Cells

scholarly journals Cordycepin reverses cisplatin resistance in human bladder cancer cells via the PTEN/PI3K/AKt pathway

2020 ◽  
Vol 19 (5) ◽  
pp. 965-970
Author(s):  
Sheng Li ◽  
Li-bin Zhou ◽  
Tie-lin Wu ◽  
Min Yin ◽  
Hui-min Long
Keyword(s):  
Flow Cytometry ◽  
Bladder Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Bladder Carcinoma ◽  
Cisplatin Resistance ◽  
Akt Signaling ◽  
Selectivity Index ◽  
Akt Signaling Pathway ◽  
Bladder Cancer Cells

Purpose: To study the influence of cordycepin (Cor) on cisplatin insensitivity in bladder carcinoma, and its underlying mechanism of action.Methods: The effects of cisplatin and Cor treatments on the viability of T24-sensitive and T24/DDPinsensitive bladder carcinoma cells were investigated by using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) method to assess selectivity index. Flow cytometry was employed to evaluate the apoptosis of T24/DDP-resistant bladder cancer cells treated with cisplatin and Cor. The concentrations of PTEN, p-AKt and Akt in T24/DDP-resistant bladder cancer cells treated with cisplatin and Cor were determined by western blot assay.Results: Compared with T24-sensitive cells, the sensitivity of T24/DDP-resistant bladder cancer cells to cisplatin was significantly decreased, along with significant increase in half-inhibitory concentration (IC50) value, resulting in 10.56-fold increase in resistance (p < 0.05). The median effective concentration (EC50) value of Cor for DDP reversal was 1.03 ± 0.15 μM, and it had a high selectivity index for normal cells (> 48.5). The results from flow cytometry showed that Cor significantly enhanced the apoptosisinducing capacity of DDP in T24/DDP-resistant cells (p < 0.05), while Western blot data indicate that PTEN protein expression increased and phosphorylated Akt protein expression decreased in T24/DDPresistantcells after Cor treatment when compared with control group (p < 0.05).Conclusion: Cordycepin significantly improves the sensitivity of T24/ DDP-resistant bladder cancer cells to cisplatin via a mechanism related to the activation of PTEN/AKt signaling pathway, thus indicating that it is a potential candidate reversing DDP-resistance in bladder cancer. Keywords: Bladder cancer, Cordycepin, Cisplatin resistance, PTEN/Akt signaling pathway

Bupivacaine modulates the apoptosis and ferroptosis in bladder cancer via PI3K/AKT pathway

2021 ◽  
Author(s):  
Jianli Hao ◽  
Weiqing Zhang ◽  
Zeqing Huang
Keyword(s):  
Bladder Cancer ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
T24 Cells ◽  
Bladder Cancer Cells ◽  
Induced Apoptosis

Abstract Background The study aimed to explore the effects of local anesthetic bupivacaine on bladder cancer cells in vivo and in vitro. Methods After T24 cells and 5637 cells were treated with different doses of bupivacaine (0-16 mM) for 24 h, MTT assay was used to detect the cytotoxicity, and bupivacaine (0.25, 0.5, 1 mM) was selected for subsequent experiments. Apoptosis was detected by Hoechst 33342 staining and TUNEL. The contents of Fe2+, MDA, GSH and ROS were detected by the corresponding kit. Mitochondrial membrane potential was detected by JC-1 kit. HE staining, TUNEL and immunohistochemistry were used to detect the xenografted tumors. Protein expression was detected by western blot. Results Bupivacaine significantly inhibited the activity of T24 cells and 5637 cells at 0.25-16 mM. Bupivacaine significantly promoted cell apoptosis with increasd concentration. bupivacaine inhibited the expression of Bcl-2 and increased the expression of Bax and cytochrome C. Moreover, bupivacaine promoted the increase of Fe2+ and ROS, and inhibited the expression of xCT and GPX4. Further results showed that bupivacaine decreased mitochondrial membrane potential, reduced GSH, and increased MDA levels. Besides, bupivacaine attenuated the phosphorylation of PI3K, Akt, and mTOR, which might be involved in the regulation of bupivacaine-induced apoptosis and ferroptosis. In addition, bupivacaine suppressed the growth of xenografted tumors, induced apoptosis and ferroptosis, and inhibited the activity of PI3K/AKT signaling pathway in xenografted tumors. Conclusion Bupivacaine could induce apoptosis and ferroptosis by inhibiting PI3K / Akt signaling pathway in bladder cancer cells.

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