Induction of apoptosis by magnolol via the mitochondrial pathway and cell cycle arrest in renal carcinoma cells

Wen, Haiyan; Zhou, Siqi; Song, Jong-Hwa

doi:10.1016/j.bbrc.2018.12.087

Cited by 26 publications

(21 citation statements)

References 20 publications

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“…The extrinsic apoptotic signal pathway is involved in Fas-FasL interaction and then activation of FADD and caspase-8, followed by caspase-3 that called the caspase-dependent pathway for causing apoptosis. Bid highly expressed will increase the ratio of BAK/Bcl-2 and affect the levels of ΔΨ m for leading to release of cytochrome c and activation of caspase-9, and caspase-3 and finally resulting in apoptosis (Jiang, Jiang, Shen, & Wang, 2014) or AIF release for causing apoptosis that are called the mitochondria-dependent pathway (Wen, Zhou, & Song, 2019). Herein, we found that ATRA combined with BDMC increased the expression of Fas when compared to ATRA or BDMC treatment alone (Figure 6c).…”

Section: F I G U R Ementioning

confidence: 75%

“…Bid highly expressed will increase the ratio of BAK/Bcl-2 and affect the levels of ΔΨ m for leading to release of cytochrome c and activation of caspase-9, and caspase-3 and finally resulting in apoptosis (Jiang, Jiang, Shen, & Wang, 2014) or AIF release for causing apoptosis that are called the mitochondria-dependent pathway (Wen, Zhou, & Song, 2019). Bid highly expressed will increase the ratio of BAK/Bcl-2 and affect the levels of ΔΨ m for leading to release of cytochrome c and activation of caspase-9, and caspase-3 and finally resulting in apoptosis (Jiang, Jiang, Shen, & Wang, 2014) or AIF release for causing apoptosis that are called the mitochondria-dependent pathway (Wen, Zhou, & Song, 2019).…”

Section: Results Frommentioning

confidence: 99%

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Combinational treatment of all‐trans retinoic acid (ATRA) and bisdemethoxycurcumin (BDMC)‐induced apoptosis in liver cancer Hep3B cells

et al. 2019

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The effects of two-drug combination, all-trans retinoic acid (ATRA) and bisdemethoxycurcumin (BDMC), on apoptosis induction of liver cancer cells were investigated in human liver Hep 3B cells. Two-drug combination caused a more effective decrease in cell viability and in induction of S phase arrest, DNA damage, and cell apoptosis than that of ATRA or BDMC only. Also, the two-drug combination caused more cells to undergo significantly increased ROS productions when compared to that of ATRA or BDMC only. Results of Western blotting demonstrated that two-drug combination increased expressions of Fas, pro-apoptotic proteins, and active form of caspase-3 and -9, but decreased that of anti-apoptotic proteins and XIAP than that of ATRA or BDMC only in Hep 3B cells. In conclusion, ATRA combined with BDMC enhance cell apoptosis and associated protein expression in Hep 3B cells. Practical applicationsBisdemethoxycurcumin (BDMC) derived from natural plants, turmeric (Curcuma longa), which had been used for Asia food for thousands of years. All-trans retinoid acid (ATRA) is currently used as a primary treatment for patients with acute

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Section: F I G U R Ementioning

confidence: 75%

Section: Results Frommentioning

confidence: 99%

Combinational treatment of all‐trans retinoic acid (ATRA) and bisdemethoxycurcumin (BDMC)‐induced apoptosis in liver cancer Hep3B cells

et al. 2019

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“…Therefore, the subsequent research focused on the molecular mechanism of GA promoting T24 cells apoptosis. Several researches showed that mitochondria can maintain cell energy supply and its dysfunction will promote apoptosis, which is associated with ROS accumulation and MMP depolarization (Song et al, 2016;Burke, 2017;Wen et al, 2019). Besides, it has been confirmed that ROS generation and MMP depolarization would change intracellular environment and cause oxidative damage even cell apoptosis (Zhang et al, 2015).…”

Section: Discussionmentioning

confidence: 97%

“…As apoptosis is initiated, mitochondria activates downstream apoptotic pathway by releasing Cytochrome C (Cyt-c), and then further activating cysteine-aspartic proteases (caspase) (Min et al, 2018). The activated caspase will directly cause intracellular proteins degradation and cytoplasmic nucleus substrates decomposition, and eventually leading to apoptosis (Wen et al, 2019). Several studies have indicated that certain drugs caused cancer cells apoptosis were closely associated with mitochondrial pathway (Song et al, 2016;Wang et al, 2016;Fan et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Gallic Acid Inhibits Bladder Cancer T24 Cell Progression Through Mitochondrial Dysfunction and PI3K/Akt/NF-κB Signaling Suppression

Zeng

et al. 2020

Front. Pharmacol.

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Gallic acid (GA), a hydrolyzable tannin, has a wide range of pharmacological activities. This study revealed that, GA significantly inhibited T24 cells viability in a concentration-and time-dependent manner. The IC 50 of GA stimulating T24 cells for 24, 48, and 72 h were 21.73, 18.62, and 11.59 µg/ml respectively, and the inhibition rate was significantly higher than the positive control drug selected for CCK-8 assay. Meanwhile, after GA treatment, the morphology of T24 cells were changed significantly. Moreover, GA significantly inhibited T24 cells proliferation and blocked T24 cells cycle in S phase (p < 0.001). GA induced T24 cells apoptosis (p < 0.001), accompanied by reactive oxygen species (ROS) accumulation and mitochondrial membrane potential (MMP) depolarization. Western blotting analysis showed that GA significantly increased Cleaved caspase-3, Bax, P53, and Cytochrome C (Cyt-c) proteins expression, and decreased Bcl-2, P-PI3K, P-Akt, P-IkBa, P-IKKa, and P-NF-kB p65 proteins expression in T24 cells (p < 0.05). Real-Time PCR results verified that GA significantly promoted Caspase-3, Bax, P53, and Cyt-c genes expression, and inhibited Bcl-2, PI3K, Akt, and NF-kB p65 genes expression (p < 0.001). However, on the basis of GA (IC 50) stimulation, NAC (an oxidative stress inhibitor) pretreatment reversed the apoptotic rate of T24 cells and the expression of Bax, Cleaved caspase-3, P53, Bcl-2 proteins, and the MMP level in T24 cells, as well as the expression of Cyt-c protein in T24 cells mitochondria and cytoplasm. In addition, GA significantly suppressed T24 cells migration and invasion ability with VEGF protein inhibition (p < 0.001). Briefly, GA can inhibit T24 cells proliferation, metastasis and promote apoptosis, and the pro-apoptotic activity is closely associated with mitochondrial dysfunction and PI3K/Akt/NF-kB signaling suppression. Our study will help in finding a safe and effective treatment for bladder cancer.

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“…Multiple studies demonstrate the anticancer function of magnolol. Magnolol induces apoptosis through regulation of the mitochondrial pathway in osteosarcoma, renal cancer and gastric adenocarcinoma [10][11][12]. Magnolol also induces cell cycle arrest and apoptosis via p21-or p27-dependent G2/M phase cell cycle arrest [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Magnolol Enhances the Therapeutic Effects of TRAIL through DR5 Upregulation and Downregulation of c-FLIP and Mcl-1 Proteins in Cancer Cells

2020

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Magnolol is a biologically active compound, isolated from the Chinese herb Magnolia, that regulates antiproliferative, anticancer, antiangiogenic and antimetastatic activities. We found that magnolol sensitizes TRAIL-induced apoptotic cell death via upregulation of DR5 and downregulation of cellular FLICE-inhibitory protein (c-FLIP) and Mcl-1 in cancer cells, but not in normal cells. Mechanistically, magnolol increased ATF4-dependent DR5 expression at the transcription level, and knockdown of ATF4 markedly inhibited magnolol-induced DR5 upregulation. Silencing DR5 with siRNA prevented combined treatment with magnolol and TRAIL-induced apoptosis and PARP cleavage. Magnolol induced proteasome-mediated Mcl-1 downregulation, while magnolol-induced c-FLIP downregulation was regulated, at least in part, by lysosomal degradation. Our results revealed that magnolol enhanced TRAIL-induced apoptosis via ATF4-dependent DR5 upregulation and downregulation of c-FLIP and Mcl-1 proteins.

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Induction of apoptosis by magnolol via the mitochondrial pathway and cell cycle arrest in renal carcinoma cells

Cited by 26 publications

References 20 publications

Combinational treatment of all‐trans retinoic acid (ATRA) and bisdemethoxycurcumin (BDMC)‐induced apoptosis in liver cancer Hep3B cells

Combinational treatment of all‐trans retinoic acid (ATRA) and bisdemethoxycurcumin (BDMC)‐induced apoptosis in liver cancer Hep3B cells

Gallic Acid Inhibits Bladder Cancer T24 Cell Progression Through Mitochondrial Dysfunction and PI3K/Akt/NF-κB Signaling Suppression

Magnolol Enhances the Therapeutic Effects of TRAIL through DR5 Upregulation and Downregulation of c-FLIP and Mcl-1 Proteins in Cancer Cells

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