Autophagy and multidrug resistance in cancer

Li, Yingjie; Lei, Yuhe; Yao, Nan; Wang, Chenran; Hu, Nan; Ye, Wen‐Cai; Zhang, Dongmei; Chen, Zhe‐Sheng

doi:10.1186/s40880-017-0219-2

Cited by 580 publications

(471 citation statements)

References 101 publications

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“…Autophagy plays a dual role in either protecting cancer cells from chemotherapy or promoting cancer cells apoptosis . Many phytochemicals including resveratrol and curcumin have been reported to inhibit tumor growth through the induction of autophagy .…”

Section: Discussionmentioning

confidence: 99%

“…Autophagy plays a dual role in either protecting cancer cells from chemotherapy or promoting cancer cells apoptosis. 51,52 Many phytochemicals including resveratrol and curcumin have been reported to inhibit tumor growth through the induction of autophagy. 53,54 Our results showed that UA increased the expression of LC3B-II and p62, which are autophagy-related biomarkers.…”

Section: Discussionmentioning

confidence: 99%

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Ursolic acid induces apoptosis and autophagy in oral cancer cells

Lin

Chin

Lee

et al. 2019

Environmental Toxicology

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Oral squamous cell carcinoma (OSCC) is the fifth common cause of cancer mortality in Taiwan with high incidence and recurrence and needs new therapeutic strategies. In this study, ursolic acid (UA), a triterpenoid, was examined the antitumor potency in OSCC cells. Our results showed that UA inhibited the proliferation of OSCC cells in a dose‐ and time‐dependent manner in both Ca922 and SCC2095 oral cancer cells. UA induced caspase‐dependent apoptosis accompanied with the modulation of various biological biomarkers including downregulating Akt/mTOR/NF‐κB signaling, ERK, and p38. In addition, UA inhibited angiogenesis as evidenced by abrogation of migration/invasion and blocking MMP‐2 secretion in Ca922 cells. Interestingly, UA induced autophagy in OSCC cells, as manifested by LC3B‐II conversion and increased p62 expression and accumulation of autophagosomes. Inhibition by autophagy inhibitor enhanced UA‐mediated apoptosis in Ca922 cells. The experiment provides a rationale for using triterpenoid in the treatment of OSCC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Lin

Chin

Lee

et al. 2019

Environmental Toxicology

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“…In addition, some other pathways such as focal adhesion, autophagy and AGE‐RAGE with high enrichment may also be involved in hypoxic cancer biology. Focal adhesion pathway changes in cancer development and cancer adhesion have been reported to be the main factors for chemotherapy resistance, while autophagy has been widely reported to take part in multidrug resistance during cancer treatment . Moreover, a novel pathway which has been reported in cancer research in recent years is AGE‐RAGE pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Focal adhesion pathway changes in cancer development and cancer adhesion have been reported to be the main factors for chemotherapy resistance, 39 while autophagy has been widely reported to take part in multidrug resistance during cancer treatment. 40 Moreover, a novel pathway which has been reported in cancer research in recent years is AGE-RAGE pathway. Hypoxia-induced glycolysis may lead to enhanced glucose uptake of tumor cells which results in accumulation of advanced glycation end products (AGE).…”

mentioning

confidence: 99%

Hypoxia induced changes in miRNAs and their target mRNAs in extracellular vesicles of esophageal squamous cancer cells

Chen

Chu

et al. 2020

Thoracic Cancer

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Background Extracellular vesicles (EVs) are endogenous membrane vesicles with a diameter of 30–200 nm. It has been reported that hypoxic cancer cells can release numerous EVs to mediate multiple regional and systemic effects in the tumor microenvironment. Methods In this study, we used ultracentrifugation to extract EVs secreted by TE‐13, an esophageal squamous carcinoma (ESCC) cell line during normoxia and hypoxia and performed high‐throughput sequencing to detect exosomal miRNAs. Gene ontology (GO) and KEGG pathway analyses were used to reveal pathways potentially regulated by the miRNAs. Results A total of 10 810 miRNAs were detected; 50 were significantly upregulated and 34 were significantly downregulated under hypoxic environment. GO analysis identified enrichment of protein binding, regulation of transcription (DNA‐templated), and membrane as molecular function, biological process, and cellular component, respectively. KEGG pathway analysis revealed cancer‐associated pathways, phospholipase D signaling pathway, autophagy, focal adhesion and AGE‐RAGE signaling as the key pathways. Further verification experiment from qRT‐PCR indicated that miR‐128‐3p, miR‐140‐3p, miR‐340‐5p, miR‐452‐5p, miR‐769‐5p and miR‐1304‐p5 were significantly upregulated in EVs from hypoxia TE‐13 cells while miR‐340‐5p was significantly upregulated in two other ESCC cells, ECA109 and TE‐1. Conclusion This study, for the first time reveals changes in the expression of exosomal miRNAs in hypoxic ESCC cells and these findings will act as a resource to study the hypoxic tumor microenvironment and ESCC EVs.

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“…On the other hand, excessive autophagy in apoptosis-deficient cells could trigger massive cell death, thereby sensitizing cancer cells to the chemodrugs. 33 Previous study has shown that USP14 could negatively regulate autophagy by removing ubiquitin chains of Lys63 from Beclin-1. 34 Thus, to explore the role of USP14 in autophagy in GC cells, we determined the levels of LC3A/B I and LC3A/B II in USP14-depleted MKN45 and KATO III cells, and observed a high ratio of LC3A/B II to LC3A/B I expression, indicating these cells were undergoing autophagy ( Figure S3).…”

Section: F I G U R E 4 Usp14 Modulated Sensitivity Of Gc Cells To Cismentioning

confidence: 99%

USP14 as a novel prognostic marker promotes cisplatin resistance via Akt/ERK signaling pathways in gastric cancer

Liu

et al. 2018

Cancer Medicine

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Gastric cancer (GC) ranks the third leading cause of global cancer mortality. Despite recent progress in surgery combined with chemotherapy, the outcomes of GC patients have barely improved. Therefore, better understanding of the molecular mechanisms involved in chemoresistance of GC may help develop novel strategies to treat this deadly disease. Previous evidence has shown aberrant expressions of USP14 in multiple malignancies, suggesting an important role of USP14 in tumorigenesis. However, its role in modulating chemoresistance in GC still remains elusive. In this study, we observed that USP14 levels were significantly increased in GC tissues compared to the paired normal tissues. Multivariate analysis demonstrated that USP14 level was an independent prognostic factor for DFS in GC patients. Silencing of USP14 promoted proteasomal degradation of p‐ERK (T202/Y204) and p‐Akt (T308/S473), thus inactivating Akt and ERK signaling pathways. Interestingly, silencing of USP14 alone was not sufficient to cause overt effects on cell growth, proliferation, and apoptosis, while resulting in significant apoptosis in the presence of cisplatin in GC cells. Thus, knockdown of USP14 sensitized GC cells to cisplatin by triggering cisplatin‐induced apoptosis via impeding Akt and ERK signaling pathways. These results revealed a novel role of USP14 in modulating chemosensitivity of GC cells, suggesting USP14 may serve as not only a prognostic marker, but also a potential therapeutic target for GC patients.

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Autophagy and multidrug resistance in cancer

Cited by 580 publications

References 101 publications

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Hypoxia induced changes in miRNAs and their target mRNAs in extracellular vesicles of esophageal squamous cancer cells

USP14 as a novel prognostic marker promotes cisplatin resistance via Akt/ERK signaling pathways in gastric cancer

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