RETRACTED: Endoplasmic reticulum stress triggered by Soyasapogenol B promotes apoptosis and autophagy in colorectal cancer

Wang, Luping; Yun, Lu; Wang, Xiaojun; Sha, Liying; Wang, Luning; Sui, Yingying; Zhang, Hui

doi:10.1016/j.lfs.2018.12.023

Cited by 13 publications

(18 citation statements)

References 29 publications

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“…Numerous active ingredients isolated from natural products have been extensively studied in relation to cancer (Kinghorn et al, 2009). Soy B, a constituent of soybean, has been shown to exert tumorsuppressive role in a variety of cancers, such as renal cell carcinoma (Wang et al, 2019a), colorectal cancer (Wang et al, 2019b), and hepatocellular carcinoma (Zhang and Popovich, 2008). Here, we examined the potential therapeutic role of Soy B in laryngeal carcinoma and elucidated its possible underlying mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Various pharmacological activities of Soy B, such as neuroprotective (Lee et al, ), anti‐inflammatory (Zha et al, ), and antiviral activities have been reported. In addition, several studies have reported the antineoplastic effect of Soy B in breast cancer (Rowlands et al, ), hepatocellular carcinoma (Zhang and Popovich, ), clear cell renal carcinoma (Wang et al, ), and colorectal carcinoma (Wang et al, ). However, to our knowledge, the effect of Soy B on laryngeal carcinoma has not been investigated yet.…”

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confidence: 99%

“…The cross talk between autophagy and apoptosis in the carcinogenesis and progression of tumor has also been proposed (Su et al, 2013). Previous studies have demonstrated that Soy B could trigger apoptotic cell death and induce autophagy in various types of cancers, such as colorectal cancer and clear cell renal cell carcinoma (Wang et al, 2019a;Wang et al, 2019b). However, whether Soy B can induce apoptosis and autophagy in laryngeal carcinoma has not been determined yet.…”

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confidence: 99%

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RETRACTED: Soyasapogenol B Attenuates Laryngeal Carcinoma Progression through Inducing Apoptotic and Autophagic Cell Death

Zhi

Song

et al. 2019

The Anatomical Record

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Soyasapogenol B (Soy B), a constituent of soybean, has been shown to exhibit antitumor activities against different types of cancers. However, to our knowledge, no studies so far have investigated the effect of Soy B in human laryngeal carcinoma. This study, therefore, aimed to determine the effect of Soy B in human laryngeal carcinoma cell lines HeP‐2 and TU212 and to elucidate the possible underlying mechanisms by which Soy B can induce its antitumor effects. The results showed that Soy B effectively attenuated the cell growth by causing G0/G1 phase cell cycle arrest in laryngeal carcinoma cell lines. Moreover, the percentage of apoptotic and autophagic cells dramatically increased upon exposure to Soy B. Western blotting results confirmed that Soy B can alter the expression levels of established markers of apoptosis and autophagy. Interestingly, both apoptosis inhibitor (ZVAD‐fmk) and autophagy inhibitor (3‐MA) could partially reverse the effect of Soy B, while blocking autophagy did not cause obvious alteration in the percentage of apoptotic cells. Similarly, in vivo studies validated that Soy B could effectively reduce the size of the tumor and induce apoptosis and autophagy in tumor tissues. Collectively, these results suggested that Soy B can exert anticancer activities against laryngeal carcinoma through inducing apoptotic and autophagic cell death. Our study highlighted the potential role of Soy B as a chemotherapeutic agent for laryngeal carcinoma. Anat Rec, 2019. © 2019 American Association for Anatomy Anat Rec, 303:1851–1858, 2020. © 2019 American Association for Anatomy

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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RETRACTED: Soyasapogenol B Attenuates Laryngeal Carcinoma Progression through Inducing Apoptotic and Autophagic Cell Death

Zhi

Song

et al. 2019

The Anatomical Record

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“…Excessive ER stress is closely linked to inhibition of cell growth and/or induction of cell apoptosis. Truly, it is demonstrated that induction of ER stress is common to many anti-cancer drugs and/ or agents [21,22]. Increasing evidence illustrates that cells undergoing ER stress are characterized by increases in expression of molecular chaperones (e.g., GRP78) [23] and phosphorylation of eIF-2α with global translation inhibition [24].…”

Section: Discussionmentioning

confidence: 99%

Cucurbitacin E’s Anti-Cancer Effects on HCT116 Human Colon Cancer Cells by Controlling Expression and Phosphorylation levels of Caspase-9, eIF-2α, and ATF-4

Yadav

Jang

2020

Keimyung Med J

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Cucurbitacin E is a pivotal member of the cucurbitacin family and has been shown to have anti-cancer effects. However, until now, the anti-cancer effect and mode of action of cucurbitacin E in human colon cancer cells remain unclear. In this study, we investigated whether cucurbitacin E inhibits the growth of HCT116 human colorectal cancer cells. Treatment of cucurbitacin E at 1 µM markedly reduced the survival of HCT116 cells. Moreover, treatment of cucurbitacin E at 1 µM caused nuclear DNA fragmentation in HCT116 cells, pointing out its apoptosis-inducing effect. Treatment of cucurbitacin E at 1 µM also led to the activation of caspase-9 and poly(ADP-ribose) polymerase (PARP) cleavage without affecting expression of death receptor (DR)-4/5 in HCT116 cells. Furthermore, while treatment of cucurbitacin E at 1 µM had no effect on expression of Mcl-1, it largely increased expression and phosphorylation of eukaryotic translation initiation factor-2α (eIF-2α) and activating transcription factor-4 (ATF-4) in HCT116 cells. Treatment of cucurbitacin E at 1 µM further up-regulated phosphorylation of extracellular signal-regulated kinase-1/2 (ERK-1/2), but not c-Jun N-terminal kinase1/2 (JNK-1/2), in HCT116 cells. However, treatment with PD98059, an inhibitor of ERK-1/2, that strongly blocked activation of ERK-1/2 had no effect on reduction of survival of HCT116 cells treated with cucurbitacin E at 1 µM. Taken together, these findings demonstrate that cucurbitacin E at 1 µM has strong anti-survival and pro-apoptotic effects on HCT116 cells, which are mediated through control of the expression and phosphorylation levels of caspase-9, PARP, eIF-2α, and ATF-4.

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“…In some circumstances, appropriate autophagy is sufficient to provide ATP to meet intracellular energy demands for cell survival. Conversely, excessive autophagy could promote apoptosis and result in autophagic cell death [23][24][25][26] .…”

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confidence: 99%

Vitamin K2 promotes PI3K/AKT/HIF-1α-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells

Duan

Mei

Yang

et al. 2020

Sci Rep

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Vitamin K2 has been shown to exert remarkable anticancer activity. However, the detailed mechanism remains unclear. Here, our study was the first to show that Vitamin K2 significantly promoted the glycolysis in bladder cancer cells by upregulating glucose consumption and lactate production, whereas inhibited TCA cycle by reducing the amounts of Acetyl-CoA. Moreover, suppression of PI3K/ AKT and HIF-1α attenuated Vitamin K2-increased glucose consumption and lactate generation, indicating that Vitamin K2 promotes PI3K/AKT and HIF-1α-mediated glycolysis in bladder cancer cells. Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Intriguingly, glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagic cell death. Furthermore, both inhibition of PI3K/AKT/HIF-1α and attenuation of glycolysis significantly blocked Vitamin K2-induced AMPK activation and subsequently prevented autophagic cell death. Collectively, these findings reveal that Vitamin K2 could induce metabolic stress and trigger AMPK-dependent autophagic cell death in bladder cancer cells by PI3K/AKT/HIF-1α-mediated glycolysis promotion. Cancer cells, including bladder carcinoma cells, display the altered metabolism, compared to normal cells 1. One of the most metabolic shifts in cancer cells is the aberrant glucose metabolism. Unlike the normal cells, most cancer cells exhibit the remarkably increased glucose uptake and glycolysis rate to meet their rapid proliferation and metastasis 2. Moreover, numerous studies indicate that the glycolysis is usually uncoupled from the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) in cancer cells. Therefore, pyruvate, the end product of glycolysis, is mainly diverted to lactate production, with the reduction of mitochondrial TCA cycle and OXPHOS 3. This metabolic shift is well-known as the Warburg effect. However, in tumor microenvironment, the nutrients including glucose are limited. Excessively increasing glycolysis will inevitably result in intracellular metabolic stress and trigger cancer cell death due to energy depletion 4. Therefore, in nutrient-deficient tumor microenvironment, the method of promoting glycolysis to induce metabolic stress and activate cell death appears to be a novel strategy for cancer treatment. Phosphatidylinositide-3-kinase (PI3K) and AKT are usually hyper-activated in cancer cells. There are accumulating evidences indicating that activation of PI3K and AKT plays a pivotal role in the regulation of aerobic glycolysis in cancer cells 5-7. The activated PI3K/AKT can directly promote the shift to the aerobic glycolysis, rendering cancer cells more reliance on glucose consumption for lactate generation 8,9. Although activation of PI3K and AKT could directly stimulate the aerobic glycolysis by positive regulation of some glycol...

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RETRACTED: Endoplasmic reticulum stress triggered by Soyasapogenol B promotes apoptosis and autophagy in colorectal cancer

Cited by 13 publications

References 29 publications

RETRACTED: Soyasapogenol B Attenuates Laryngeal Carcinoma Progression through Inducing Apoptotic and Autophagic Cell Death

RETRACTED: Soyasapogenol B Attenuates Laryngeal Carcinoma Progression through Inducing Apoptotic and Autophagic Cell Death

Cucurbitacin E’s Anti-Cancer Effects on HCT116 Human Colon Cancer Cells by Controlling Expression and Phosphorylation levels of Caspase-9, eIF-2α, and ATF-4

Vitamin K2 promotes PI3K/AKT/HIF-1α-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells

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