TRPC5OS induces tumorigenesis by increasing ENO1-mediated glucose uptake in breast cancer

Cui, Yangyang; Peng, Jinghui; Zheng, Mingzhe; Ge, Huan; Wu, Xiaowei; Xia, Yiqin; Huang, Yue; Wang, Shui; Yin, Yongmei; Fu, Ziyi; Xie, Hui

doi:10.1016/j.tranon.2022.101447

Cited by 9 publications

(2 citation statements)

References 44 publications

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“…It has been suggested that a high blood glucose microenvironment upregulates the expression of sterol regulatory element-binding protein 1 (SREBP1), resulting in accelerated cell proliferation and cancer progression compared to normal blood glucose levels [ 45 ]. Increased glucose metabolism via glycolysis upregulates the expression of transient receptor potential channel 5 opposite strand (TRPC5OS) mRNA, leading to activated cancer cell proliferation and tumorigenesis in breast cancer cells [ 10 ]. Increased glucose uptake and glycolytic flux reported in prostate cancer cells have been suggested to be associated with an upregulation of glucose transporter protein-1 (GLUT1) expression [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

“…The metabolic shift of cancer cells, or the “Warburg effect,” demonstrates enhanced anaerobic metabolism of ATP synthesis under conditions without dependence on the supply of oxygen that leads to increased lactate production. Overexpression of transient receptor potential channel 5 (TRPC5) in breast cancer cells enhances glucose absorption via glucose transporter protein (GLUT) upregulation, which is correlated with the PI3K/Akt pathway and leads to enhanced breast carcinogenesis [ 10 ]. The overexpression of GLUT1 in gastric cancer cells improves glucose uptake and consumption, elevates lactate and ATP production, and ultimately stimulates cell proliferation [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Enhanced apoptosis of HCT116 colon cancer cells treated with extracts from Calotropis gigantea stem bark by starvation

Simanurak,

Pekthong,

Somran

et al. 2023

Heliyon

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Enhanced apoptosis of HCT116 colon cancer cells treated with extracts from Calotropis gigantea stem bark by starvation

Simanurak,

Pekthong,

Somran

et al. 2023

Heliyon

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Microproteins/micropeptides dysregulation contributes to cancer progression and development: A mechanistic review

Rodrigues,

Bangali,

Ali

et al. 2024

Cell Biology International

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Microproteins, known as micropeptides, are small protein molecules encoded by short open reading frames. These recently identified molecules have been proven to be an essential part of the human proteome that participates in multiple processes, such as DNA repair, mitochondrial respiration, and regulating different signaling pathways. A growing body of studies has evidenced that microproteins exhibit dysregulated expression levels in various malignancies and contribute to tumor progression. It has been reported that microproteins interact with many proteins, such as enzymes (e.g., adenosine triphosphate synthase) and signal transducers (e.g., c‐Jun), and regulate malignant cell metabolism, proliferation, and metastasis. Moreover, microproteins have been found to play a significant role in multidrug resistance in vitro and in vivo by their activity in DNA repair pathways. Considering that, this review intended to summarize the roles of microproteins in different aspects of tumorigenesis with diagnostic and therapeutic perspectives.

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Knockdown of ENO1 promotes autophagy dependent‐ferroptosis and suppresses glycolysis in breast cancer cells via the regulation of CST1

Huang,

Lu,

You

et al. 2024

Drug Development Research

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Autophagy‐dependent ferroptosis and glycolysis play a significant role in tumor development. α‐Enolase (ENO1), a glycolytic enzyme, has been demonstrated to function as a crucial modulator in breast cancer (BC). However, the specific mechanism by which ENO1 influences the ferroptosis and glycolysis of BC remains unclear. qRT‐PCR, along with western blot analysis was applied to investigate ENO1 and cystatin SN (CST1) expression in BC cells. Glycolysis level was measured by extracellular acidification rate (ECAR), lactate production, glucose consumption, and western blot analysis. Ferroptosis was evaluated by iron and lipid peroxidation assay, DCFH‐DA staining, and western blot analysis. Immunofluorescence, together with western blot analysis was adopted for assessing cell autophagy and mTOR signaling pathway. Cell apoptosis and Ki67 level were measured by TUNEL and immunohistochemistry, respectively. ENO1 had abundant existence in BC cell lines. ENO1 silencing inhibited glycolysis but promoted ferroptosis and autophagy. In addition, autophagy inhibitor 3‐MA reversed the impacts of ENO1 silencing on glycolysis and ferroptosis. Meanwhile, mTOR activator MHY1485 demonstrated opposing effects on autophagy. Moreover, CST1 could be extensively found in BC cell lines, and its overexpression reversed the effects of ENO1 silencing on glycolysis and ferroptosis. In vivo experiments illustrated that ENO1 deletion suppressed BC tumor growth, increased the apoptosis rate, restrained cell proliferation, and glycolysis, but promoted ferroptosis and autophagy, as well as reducing CST1 and mTOR signaling. To sum up, ENO1 silencing mediated a utophagy‐dependent ferroptosis and glycolysis in BC cells by regulating CST1.

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TRPC5OS induces tumorigenesis by increasing ENO1-mediated glucose uptake in breast cancer

Cited by 9 publications

References 44 publications

Enhanced apoptosis of HCT116 colon cancer cells treated with extracts from Calotropis gigantea stem bark by starvation

Enhanced apoptosis of HCT116 colon cancer cells treated with extracts from Calotropis gigantea stem bark by starvation

Microproteins/micropeptides dysregulation contributes to cancer progression and development: A mechanistic review

Knockdown of ENO1 promotes autophagy dependent‐ferroptosis and suppresses glycolysis in breast cancer cells via the regulation of CST1

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