Endoplasmic reticulum stress targeted therapy for breast cancer

Xu, Di; Liu, Zhen; Liang, Mingxing; Fei, Yin-Jiao; Zhang, Wei; Wu, Yang; Tang, Jinhai

doi:10.1186/s12964-022-00964-7

Cited by 20 publications

(14 citation statements)

References 101 publications

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“…ER stress is a double-edged sword ( 17 ). On the one hand, ER stress is important for tumor microenvironmental homeostasis and tumor growth inhibition; on the other hand, sustained ER stress can initiate multiple signaling pathways to promote tumor cell death ( 18 ).…”

Section: Discussionmentioning

confidence: 99%

Norcantharidin inhibits the malignant progression of cervical cancer by inducing endoplasmic reticulum stress

Zhang,

Sun,

et al. 2024

Mol Med Rep

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The antitumor effect of norcantharidin (NCTD) has been widely reported. However, whether NCTD can inhibit cervical cancer remains unknown. In the present study, it was shown that NCTD inhibited the viability of cervical cancer cells and caused cell cycle arrest in a concentration-dependent manner. Further analysis revealed that the NCTD-induced reduction in cell viability could be reversed by the inhibitor of apoptosis z-VAD-FMK and by the inhibitor of endoplasmic reticulum (ER) stress, 4-phenylbutyric acid (4-PBA). Additionally, NCTD led to the accumulation of reactive oxygen species as well as a decrease in the mitochondrial membrane potential in cervical cancer cells, whereas 4-PBA pre-treatment attenuated these alterations. In addition, NCTD increased the expression of the apoptosis-related proteins Bip, activating transcription factor (ATF) 4 and C/EBP homologous protein in a concentration-dependent manner. Moreover, NCTD significantly increased the expression of the ER stress-related signaling molecules protein kinase R-like ER kinase, inositol-requiring enzyme 1 and ATF6, but 4-PBA abolished these effects. In vivo experiments showed that NCTD significantly inhibited the growth of subcutaneous tumors in mice. Additionally, the expression of ER stress-related molecules and apoptosis-related proteins increased significantly after NCTD treatment. In conclusion, NCTD induces apoptosis by activating ER stress and ultimately curtails the progression of cervical cancer.

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Section: Discussionmentioning

confidence: 99%

Norcantharidin inhibits the malignant progression of cervical cancer by inducing endoplasmic reticulum stress

Zhang,

Sun,

et al. 2024

Mol Med Rep

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“…A large number of studies have shown that ER stress is involved in many diseases, such as central nervous system diseases, in ammation, cancer, and so on [15]. In cancer cells, ER stress may activate autophagy, degrade misfolded proteins in cells and reuse them, which is a way to survive under stress, therefore, ER stress has become a therapeutic target for the treatment of many cancers [16,17]. Autophagy is an evolutionarily conserved membrane transport and degradation process, which operates at basal levels under normal conditions as a means of degrading cytosolic proteins and organelles.…”

Section: Discussionmentioning

confidence: 99%

Ginsenosides Rh2 and Rg3 exert their anti-cancer effects on non-small cell lung cancer by regulating cell autophagy and choline-phosphatidylcholine metabolism

Chen

Qiu

Wang

et al. 2023

Preprint

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Background: Ginseng (Panax ginseng C. A. Meyer) herb itself and its derived preparations (e.g. Shenmai injection) are often prescribed for cancer patients as Traditional Chinese Medicines clinically in China. Ginsenosides Rh2 and Rg3 are two of main active components of ginseng. They have significant cytotoxic effect against non-small cell lung cancer (NSCLC), but the mechanisms are not very clear, especially lack of research on the combination of cell autophagy and metabolism. This study explores the mechanism of ginsenosides Rh2 and Rg3 against NSCLC from these two aspects. Methods: In this study, we investigated the regulatory effects of ginsenosides Rh2 and Rg3 on cellular autophagy and metabolism in non-small cell lung cancer cell lines. Their regulations of cellular autophagy were detected by immunofluorescence, MDC staining, and transmission electron microscopy, while their regulations of cellular metabolism were detected by cellular metabolomics. Results: Our results showed that ginsenosides Rh2 and Rg3 can significantly induce cell autophagy, and can lead to autophagic cell death through endoplasmic reticulum stress-autophagy axis, similar to ginseng total ginsenosides extract (TGS). They also significantly regulate the cell metabolome at the same time. The regulatory effect of ginsenosides Rh2 and Rg3 on the metabolism of choline-phosphatidylcholinemay be the cellular metabolic mechanism of their cytotoxicity. Conclusion: Our findings suggested that ginsenosides Rh2 and Rg3 could induce autophagic cell death and regulate choline-phosphatidylcholine metabolism in NSCLC cells. This study has a new understanding of the antitumor mechanism of ginsenosides Rh2 and Rg3, and suggests a new direction of studying the pharmacological mechanism of natural active components.

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“…During cellular homeostasis, this protein on ER binds to molecular chaperone Glucose‐regulated protein 78 (GRP78). However, during ER stress, GRP78 gets separated from these proteins and is actively recruited to accumulate misfolded proteins (Bae et al, 2021; Cui et al, 2022; Xu et al, 2022; Zeng et al, 2020).…”

Section: Anticancer Activity Of Curcumin Analogues Via Different Mole...mentioning

confidence: 99%

Mechanism insights of curcumin and its analogues in cancer: An update

Joshi,

Verma,

Kumar Semwal

et al. 2023

Phytotherapy Research

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Cancer is the world's second leading cause of mortality and one of the major public health problems. Cancer incidence and mortality rates remain high despite the great advancements in existing therapeutic, diagnostic, and preventive approaches. Therefore, a quest for less toxic and more efficient anti‐cancer strategies is still at the forefront of the current research. Traditionally important, curcumin commonly known as a wonder molecule has received considerable attention as an anti‐cancer, anti‐inflammatory, and antioxidant candidate. However, limited water solubility and low bioavailability restrict its extensive utility in different pathological states. The investigators are making consistent efforts to develop newer strategies to overcome its limitations by designing different analogues with better pharmacokinetic and pharmacodynamic properties. The present review highlights the recent updates on curcumin and its analogues with special emphasis on various mechanistic pathways involved in anti‐cancer activity. In addition, the structure–activity relationship of curcumin analogues has also been precisely discussed. This article will also provide key information for the design and development of newer curcumin analogues with desired pharmacokinetic and pharmacodynamic profiles and will provide in depth understanding of molecular pathways involved in the anti‐cancer activities.

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Endoplasmic reticulum stress targeted therapy for breast cancer

Cited by 20 publications

References 101 publications

Norcantharidin inhibits the malignant progression of cervical cancer by inducing endoplasmic reticulum stress

Norcantharidin inhibits the malignant progression of cervical cancer by inducing endoplasmic reticulum stress

Ginsenosides Rh2 and Rg3 exert their anti-cancer effects on non-small cell lung cancer by regulating cell autophagy and choline-phosphatidylcholine metabolism

Mechanism insights of curcumin and its analogues in cancer: An update

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