Propofol induces endoplasmic reticulum (ER) stress and apoptosis in lung cancer cell H460

Cui, Weicheng; Liu, Yan; Zhu, Yongqiang; Song, Tao; Wang, Qiushi

doi:10.1007/s13277-014-1677-7

Cited by 48 publications

(44 citation statements)

References 16 publications

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“…Caspase-3 is a cysteine protease, which are pro-apoptotic proteins with prominent roles in ERS-induced cell death [42, 43]. ERS is well-characterized in human LC [44, 45]. Recent evidence has suggested that ERS can initiate internal pathways that may induce cellular death [27].…”

Section: Discussionmentioning

confidence: 99%

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Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells

Gan

Zhou

Zhong

et al. 2017

Cell Physiol Biochem

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Background/Aims: Lung cancer (LC) continues to be one of the most prevalent cancers around the world. During this study we aimed to investigate the involvement of endoplasmic reticulum stress (ERS) in autophagy, apoptosis, and chemotherapy resistance of mutant p53 LC cells. Methods: Immunohistochemistry was employed to help determine the p53 mutation status of cancer cells from 92 primary LC patients, who were subsequently assigned to either the mutant p53 (n = 39) or wild-type p53 group (n = 53). Results: Mutant p53 cells exhibited increased expression of the C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78), and inositol-requiring enzyme-1α (IRE1α). The Mutant p53 cells were also found to be sensitive to chemotherapy and displayed decreased expression of PI3K, Akt, and mTOR. The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR. Both agents increased the expression of CHOP, GRP78, IRE1α, LC3-II/LC3-I, Atg5, Atg7, caspase-3, caspase-12, cleaved caspase-3, cleaved caspase-12, as well as decreases in cell proliferation as well as the expression levels of PI3K, Akt, and mTOR. Enhanced levels of cell apoptosis and reduced chemotherapy resistance were also detected. Conclusion: The findings of our study suggest that ERS promotes autophagy and apoptosis, while acting to reduce chemotherapy resistance in mutant p53 LC cells by downregulating the PI3K/Akt/mTOR signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…Calcium imbalance or aberrant protein folding in the ER result in ERS and induce cell destruction responses [47, 48]. Alterations in the ER molecular chaperone levels can suppress tumor growth in vivo [44]. Likewise, ERS-induced apoptosis is also highly dependent on the upregulation of CHOP [49].…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells

Gan

Zhou

Zhong

et al. 2017

Cell Physiol Biochem

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“…Previous study revealed that propofol could inhibit cancer growth and invasion through Wnt/β‐catenin pathway . Through inducing endoplasmic reticulum stress, propofol increased cell apoptosis in lung cancer . Moreover, propofol could also suppress the pancreatic cancer proliferation and invasion via microRNA‐133a .…”

Section: Discussionmentioning

confidence: 99%

“…11 Through inducing endoplasmic reticulum stress, propofol increased cell apoptosis in lung cancer. 13 Moreover, propofol could also suppress the pancreatic cancer proliferation and invasion via microRNA-133a. 14 Besides, propofol has also been reported to inhibit the colon cancer invasion, via downregulation of MMP-2 and MMP-9.…”

Section: Discussionmentioning

confidence: 99%

“…10 Besides, recent studies even found that propofol also exerts antitumor activities in several types of cancers, such as breast cancer, lung cancer, pancreatic cancer, hepatocellular carcinoma, and colon cancer. [11][12][13][14][15] Although some of the results remain controversial, overall, propofol has been considered to possesses an antitumor role on the proliferation, invasion, and metastasis of tumor cells via regulating key RNAs and signaling pathways. 10 However, the underlying mechanisms about how propofol suppresses the development of colon cancer remain unclear.…”

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confidence: 99%

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Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF‐1 and suppressing Wnt pathway

Zhang

Zhou

et al. 2020

Cancer Medicine

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Background In the present study, we aim to investigate the potential role of propofol in the tumor progression of colon cancer. Methods Human colon cancer cell lines were cultured and exposed with 8 μg/mL propofol. RNA interference was performed to silence the expression of HOTAIR or STAT3 to explore their biological functions in colon cancer. Cell apoptosis and invasion were assessed using flow cytometry and transwell assays, respectively. Quantitative real‐time PCR, western blot, and immunohistochemistry were subjected to measure the expression patterns of HOTAIR, STAT3, Wnt signaling factors, and epithelial‐mesenchymal transition‐related markers, respectively. Besides, nude mice were transplanted with colon cancer cells for further exploration. Tumor formation, volume, and weight were evaluated to validate the in vitro findings. Results Propofol treatment promoted cell apoptosis and inhibited cell invasion in colon cancer cells, while the effects were reversed by HOTAIR overexpression. Additionally, STAT3 positively regulated HOTAIR expression, which was also negatively modulated by propofol. Moreover, STAT3 and HOTAIR were shown to independently regulate colon cancer cell apoptosis and invasion. Furthermore, HOTAIR could stimulate Wnt signaling pathway via inhibiting WIF‐1 expression and upregulating β‐catenin expression, which was also demonstrated by in vivo study. Conclusion Taken together, the current study demonstrated that propofol exerts the inhibition on cell invasion and promotion on cell apoptosis through regulating STAT3/HOTAIR by activating WIF‐1 and suppressing Wnt pathway, indicating that propofol might serve as a therapeutic role for colon cancer patients in the future.

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Propofol‐induced miR‐219‐5p inhibits growth and invasion of hepatocellular carcinoma through suppression of GPC3‐mediated Wnt/β‐catenin signalling activation

Gong

Xue

Deng

et al. 2019

J of Cellular Biochemistry

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Propofol is one of the most extensively used intravenous anaesthetic agents, which has been found to improve the surgical intervention outcome of several types of cancer, including hepatocellular carcinoma (HCC). Additionally, in vitro and in vivo experiments have also indicated that propofol affects the biological behaviour of HCC. However, the underlying mechanisms of the surgical resection of HCC with propofol have not been fully understood. In the present study, we aimed to investigate the underlying mechanism of propofol inhibition of the growth and invasion of HCC cells. Our results showed that treatment with propofol suppressed the proliferation, invasion and migration of HCC in vitro. The subcutaneous xenograft tumour and orthotopic xenograft tumour experiments in nude mice showed that propofol significantly decreased tumour volumes, growth rates and the liver orthotopic xenograft tumour in vivo. Furthermore, the underlying mechanism investigations of the suppressive effects of propofol on HCC cells revealed that propofol treatment upregulated the expression levels of the candidate tumour suppressor miR‐219‐5p. Silencing of propofol‐induced miR‐219‐5p using anti‐miR‐219‐5p abrogated the inhibitory effects on the proliferation, migration and invasion of HCC cells exerted by propofol treatment. Additionally, we demonstrated that propofol reversed the epithelial‐mesenchymal transition of Huh7 and SMMC7721 cells via miR‐219‐5p induction. The molecular mechanism behind these findings is that propofol‐induced miR‐219‐5p inhibits HCC cell progression by targeting glypican‐3 and subsequently results in the inhibition of Wnt/β‐catenin signalling. Taken together, our study provides new insights into the advantages of the surgical intervention of HCC with propofol anaesthetization.

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Propofol induces endoplasmic reticulum (ER) stress and apoptosis in lung cancer cell H460

Cited by 48 publications

References 16 publications

Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells

Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells

Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF‐1 and suppressing Wnt pathway

Propofol‐induced miR‐219‐5p inhibits growth and invasion of hepatocellular carcinoma through suppression of GPC3‐mediated Wnt/β‐catenin signalling activation

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