Retrograde signaling from autophagy modulates stress responses

Simon, Hans‐Uwe; Friis, Robert R.; Tait, Stephen W.G.; Ryan, Kevin M.

doi:10.1126/scisignal.aag2791

Cited by 67 publications

(43 citation statements)

References 111 publications

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“…MDC staining and TEM both displayed the ultrastructural features of autophagy in these cells ( Figure 3 a,b). The results of genes showed that the expression of Atg 5, Atg 7, and beclin-1 was increased after treating with 20(S)-GRh2 in U937 and K562 cells ( Figure 3 c), and were consistent with the previous studies [ 53 , 54 , 55 ]. LC3, which is a recognized indicator of autophagy evaluation and measurement, is widely used by many autophagy researchers.…”

Section: Discussionsupporting

confidence: 91%

20(S)-Ginsenoside Rh2 Induce the Apoptosis and Autophagy in U937 and K562 Cells

Zhuang

Yin

et al. 2018

Nutrients

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Acute myeloid leukemia (AML) and Chronic myelogenous leukemia (CML) are common leukemia in adults. 20(S)-GRh2 is an important bioactive substance that is present in Panax ginseng. However, there are no investigations that deal with the comparison of apoptosis, the occurrence of autophagy, and the relationship between apoptosis and autophagy after being treated with 20(S)-GRh2 in AML and CML. In this study, we explored the effect of 20(S)-GRh2 on the AML and CML (U937 and K562). Fluorescence microscopy, CCK-8, Quantitative realtime PCR, Western blot, transmission electron microscopy (TEM), and flow cytometric analysis were used to detect the occurrence of cell proliferation inhibition, apoptosis, and autophagy. By using the above methods, it was determined that apoptosis induced by 20(S)-GRh2 was more obvious in K562 than U937 cells and 20(S)-GRh2 could generate autophagy in K562 and U937 cells. When pretreated by a specific inhibitor of autophagy, (3-methyladenine), the 20(S)-GRh2-induced apoptosis was enhanced, which indicated that 20(S)-GRh2-induced autophagy may protect U937 and K562 cells from undergoing apoptotic cell death. On the other hand, pretreated by an apoptosis suppressor (Z-VAD-FMK), it greatly induced the autophagy and partially prevented 20(S)-GRh2 induced apoptosis. This phenomenon indicated that 20(S)-GRh2-induced autophagy may serve as a survival mechanism and apoptosis and autophagy could act as partners to induce cell death in a cooperative manner. These findings may provide a rationale for future clinical application by using 20(S)-GRh2 combined autophagy inhibitors for AML and CML.

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Section: Discussionsupporting

confidence: 91%

20(S)-Ginsenoside Rh2 Induce the Apoptosis and Autophagy in U937 and K562 Cells

Zhuang

Yin

et al. 2018

Nutrients

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“…Furthermore, Res induced autophagy partially through ROS. AMPK-mTOR is a classic regulatory signaling pathway in autophagy (34). However, in the experiments performed in the present study, Res did not affect AMPK and mTOR, indicating that Res induced non-classical autophagy.…”

Section: Discussioncontrasting

confidence: 69%

Autophagy suppresses resveratrol‑induced apoptosis in renal cell carcinoma 786‑O cells

Yao

Fan

2020

Oncol Lett

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As a polyphenolic compound, resveratrol (Res) is widely distributed in a variety of plants. Previous studies have demonstrated that Res can inhibit various different types of tumor growth. However, its role in renal cell carcinoma (RCC) remains largely unknown. The present study first demonstrated that Res inhibited cell viability and induced apoptosis in RCC 786-O cells. Further experiments revealed that Res damaged the mitochondria and activated caspase 3. In contrast, Z-VAD-FMK, a pan-caspase inhibitor, suppressed Res-induced apoptosis. Reactive oxygen species (ROS) were involved in the process of Res-induced apoptosis, and antioxidant N-acetyl cysteine could significantly attenuate this. Furthermore, Res activated c-Jun N-terminal kinase via ROS to induce autophagy, whereas inhibition of autophagy with chloroquine or Beclin 1 small interfering RNA aggravated Res-induced apoptosis, indicating that autophagy served as a pro-survival mechanism to protect 786-O cells from Res-induced apoptosis. Therefore, a combination of Res and autophagy inhibitors could enhance the inhibitory effect of Res on RCC.

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“…Depending on the context, it can also inhibit autophagy. 84,85 As there are a growing number of studies in autophagy and its cytoprotective effect, there might be a chance to help cancer therapeutic approaches with agents that inhibit autophagy. 86,87…”

Section: Change Of Autophagy Pathwaysmentioning

confidence: 99%

<p>A Review of Research Progress in Multidrug-Resistance Mechanisms in Gastric Cancer</p>

Ruan¹,

Liu²,

Tao³

et al. 2020

OTT

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Gastric cancer is one of the most common malignant tumors, and it is also one of the leading causes of cancer death worldwide. Because of its insidious symptoms and lack of early dictation screening, many cases of gastric cancer are at late stages which make it more complicated to cure. For these advanced-stage gastric cancers, combination therapy of surgery, chemotherapy, radiotherapy and target therapy would bring more benefit to the patients. However, the drug-resistance to the chemotherapy restricts its effect and might lead to treatment failure. In this review article, we discuss the mechanisms which have been found in recent years of drug resistance in gastric cancer. And we also want to find new approaches to counteract chemotherapy resistance and bring more benefits to the patients.

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Retrograde signaling from autophagy modulates stress responses

Cited by 67 publications

References 111 publications

20(S)-Ginsenoside Rh2 Induce the Apoptosis and Autophagy in U937 and K562 Cells

20(S)-Ginsenoside Rh2 Induce the Apoptosis and Autophagy in U937 and K562 Cells

Autophagy suppresses resveratrol‑induced apoptosis in renal cell carcinoma 786‑O cells

<p>A Review of Research Progress in Multidrug-Resistance Mechanisms in Gastric Cancer</p>

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