BCL-2 proteins and apoptosis: Recent insights and unknowns

Edlich, Frank

doi:10.1016/j.bbrc.2017.06.190

Cited by 451 publications

(302 citation statements)

References 111 publications

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“…22,23 Mitochondrial-related apoptosis F I G U R E 4 Fuziline inhibits ISO-induced endoplasmic reticulum stress in H9c2 cells. 25,26 Among them, anti-apoptotic proteins, such as Bcl-2 and Bcl-xl, mainly exist in mitochondrial membrane, while other members, such as Bid and Bax, mainly exist in cytoplasm. B-F, Quantitative analysis of the ratios of Chop/ GAPDH, p-eIF2α/eIF2α, ATF4/GAPDH, GPR 78/GAPDH and p-PERK/PERK by densitometry based on immunoblot images.…”

Section: Discussionmentioning

confidence: 99%

“…24 According to roles of Bcl-2 family in apoptosis, they can be divided into two categories: anti-apoptotic members (eg, Bcl-2 and Bcl-xl) and pro-apoptotic members (eg, Bax and Bak). 25,26 Among them, anti-apoptotic proteins, such as Bcl-2 and Bcl-xl, mainly exist in mitochondrial membrane, while other members, such as Bid and Bax, mainly exist in cytoplasm. 27 When cells receive apoptotic-related signals, Bax will reposition on the surface of mitochondria to form a pore across the mitochondrial membrane, resulting in a decrease of membrane potential and an increase of membrane permeability, thereby mitochondria will release apoptotic factors, such as cytochrome C to induce apoptosis in cells.…”

Section: Discussionmentioning

confidence: 99%

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Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Fan

Yao

et al. 2019

J Cellular Molecular Medi

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Fuziline, an aminoalcohol-diterpenoid alkaloid derived from Aconiti lateralis radix preparata, has been reported to have a cardioprotective activity in vitro. However, the potential mechanism of fuziline on myocardial protection remains unknown. In this study, we aimed to explore the efficacy and mechanism of fuziline on isoproterenol (ISO)-induced myocardial injury in vitro and in vivo. As a result, fuziline effectively increased cell viability and alleviated ISO-induced apoptosis. Meanwhile, fuziline significantly decreased the production of ROS, maintained mitochondrial membrane potential (MMP) and blocked the release of cytochrome C, suggesting that fuziline could play the cardioprotective role through restoring the mitochondrial function.Fuziline also could suppress ISO-induced endoplasmic reticulum (ER) stress via the PERK/eIF2α/ATF4/Chop pathway. In addition, using ROS scavenger NAC could decrease ISO-induced apoptosis and block ISO-induced ER stress, while PERK inhibitor GSK2606414 did not reduce the production of ROS, indicating that excess production of ROS induced by ISO triggered ER stress. And fuziline protected against ISO-induced myocardial injury by inhibiting ROS-triggered ER stress. Furthermore, fuziline effectively improved cardiac function on ISO-induced myocardial injury in rats. Western blot analysis also showed that fuziline reduced ER stress-induced apoptosis in vivo. Above these results demonstrated that fuziline could reduce ISO-induced myocardial injury in vitro and in vivo by inhibiting ROS-triggered ER stress via the PERK/eIF2α/ATF4/Chop pathway. K E Y W O R D Sapoptosis, ER stress, fuziline, isoproterenol, ROS | 1333 FAN et Al.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Fan

Yao

et al. 2019

J Cellular Molecular Medi

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“…The proliferation, apoptosis, migration and invasion of tumor cells involves a series of signaling pathways, making it a complex process with particular mechanisms that require further investigation. Bcl-2 family proteins are the most important regulatory factors in the mitochondrial apoptosis pathway and are made up of two primary groups: Apoptosis-inducing (apoptotic) proteins, including Bax, Bcl-2 antagonist/killer 1 and peptidyl-tRNA hydrolase 2, andapoptosis-inhibiting (antiapoptotic) proteins, including Bcl-2 and Bcl-2-like 1 (21)(22)(23). It was previously reported that isofraxidin significantly reduced the expression of the antiapoptotic protein Bcl-2 in colon cancer cells and increased the expression of the apoptotic proteinscaspase-3, caspase-9 and Bax (9).…”

Section: Discussionmentioning

confidence: 99%

Anticancer effects of isofraxidin against A549 human lung cancer cells via the EGFR signaling pathway

et al. 2018

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Lung cancer is the leading cause of mortality due to tumor malignancy worldwide. In recent years, the treatment of lung cancer with chemotherapy has demonstrated notable resistance and insensitivity. Therefore, it is of great importance to investigate anti‑lung cancer drugs with high efficiency and low toxicity. In the present study, the effects of isofraxidin on lung cancer cells and the associated mechanisms were investigated. The results revealed that, in vivo and in vitro, isofraxidin exhibited marked inhibitory effects on the A549 lung cancer cell line. The results of Cell Counting kit‑8, Transwell migration and Matrigel invasion assays, and flow cytometry to determine apoptosis, revealed that isofraxidin significantly inhibited the proliferation, migration and invasion of A549 cells, and induced the cell apoptosis. Furthermore, western blot analysis demonstrated that isofraxidin treatment led to effects on the expression of apoptosis‑associated proteins, including members of the Bcl‑2 protein family, and invasion‑associated proteins, including matrix metallopeptidase (MMP)‑2 and MMP‑9, which may occur via inhibition of the expression of phosphorylated (p)‑epidermal growth factor receptor, p‑AKT and p‑extracellular signal‑regulated kinase. This regulation of protein expression may contribute to the inhibition of proliferation, migration and invasion of A549lung cancer cells by isofraxidin. In addition, despite the inhibitory effects on the A549 lung cancer cell line, the present study revealed that isofraxidin exhibited low toxicity towards BEAS‑2B normal lung epithelial cells within a certain dose range (0‑160 µM), indicating that isofraxidin may be employed for lung cancer treatment with hypotoxicity and fewer side effects. In conclusion, isofraxidin may be a novel candidate for anti‑lung cancer chemotherapy.

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“…c-Myc is a key protein associated with metabolism, proliferation and oncogenesis of cancers [28], which could be modulated by lncRNA to influence cell viability [29]. Bax is an important member of Bcl-2 family, which displays pro-apoptotic role in cancers through intrinsic apoptosis pathway [30]. Moreover, MMP9 has been regarded as an essential marker for metastasis of cancers, including gastric cancer [31,32].…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00483 promotes gastric cancer development through regulating MAPK1 expression by sponging miR-490-3p

Luo

Liang

2020

Biol Res

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Background: Previous studies have shown that long noncoding RNA (lncRNA) LINC00483 was aberrantly expressed in human cancers, including gastric cancer. However, the regulatory mechanism of this lncRNA in gastric cancer remains largely unknown. The present study aimed to investigate the effect of LINC00483 on gastric cancer development and explore the potential regulatory network of LINC00483/microRNA (miR)-490-3p/mitogen-activated protein kinase 1 (MAPK1). Methods:Thirty patients with gastric cancer were recruited for tissues collection. The expression levels of LINC00483, miR-490-3p and MAPK1 were detected by quantitative real-time polymerase chain reaction or western blot. Cell viability, apoptosis, migration and invasion were determined by MTT, flow cytometry, transwell assays and western blot, respectively. The target association between miR-490-3p and LINC00483 or MAPK1 was confirmed by luciferase reporter assay. Xenograft model was established to assess the function of LINC00483 in vivo.Results: LINC00483 and MAPK1 levels were increased in gastric cancer tissues and cells. Knockdown of LINC00483 or MAPK1 inhibited cells viability, migration and invasion but promoted apoptosis in gastric cancer cells. Moreover, MAPK1 overexpression attenuated the effect of LINC00483 knockdown on gastric cancer development. LINC00483 could increase MAPK1 expression by competitively sponging miR-490-3p. miR-490-3p overexpression suppressed gastric cancer development, which was abated by introduction of LINC00483. Besides, inhibition of LINC00483 decreased xenograft tumor growth by regulating miR-490-3p/MAPK1 axis. Conclusion:Knockdown of LINC00483 inhibited gastric cancer development in vitro and in vivo by increasing miR-490-3p and decreasing MAPK1, elucidating a novel mechanism for understanding the development of gastric cancer.

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BCL-2 proteins and apoptosis: Recent insights and unknowns

Cited by 451 publications

References 111 publications

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Anticancer effects of isofraxidin against A549 human lung cancer cells via the EGFR signaling pathway

LncRNA LINC00483 promotes gastric cancer development through regulating MAPK1 expression by sponging miR-490-3p

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