Caveolin‐1 increases glycolysis in pancreatic cancer cells and triggers cachectic states

Hu, Lijuan; Xu, Xiaoqing; Li, Qiuju; Chen, Xijuan; Yuan, Xia; Qiu, Shuai; Yao, Chuanshan; Zhang, David; Wang, Feng

doi:10.1096/fj.202100121rrr

Cited by 19 publications

(36 citation statements)

References 40 publications

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“…For example, long noncoding RNA SNHG11 facilitates prostate cancer progression by upregulating IGF1R expression 27 . IGF1R increases the proliferation and glycolysis of pancreatic cancer 28 . HOXB13 accelerates gastric cancer cell migration and invasion by upregulating the expression of IGF1R 29 .…”

Section: Discussionmentioning

confidence: 99%

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Circular RNA circ_0001459 accelerates hepatocellular carcinoma progression via the miR‐6165/IGF1R axis

Shen

Zhao

Zeng

et al. 2022

Annals of the New York Academy of Sciences

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An increasing amount of evidence shows that circular RNAs (circRNAs) have critical effects on cancer progression and development; however, the biological function and potential molecular mechanism of circRNAs in hepatocellular carcinoma (HCC) are still unclear. CircRNA sequencing was used to identify differentially expressed circRNAs between HCC tissue and adjacent normal tissue. We found that circ_0001459 expression was significantly elevated in HCC tissue and cell lines. Furthermore, in vitro and in vivo functional experiments were carried out to detect the effects of circ_0001459 on HCC growth and metastasis. Knockdown of circ_0001459 significantly inhibited the proliferation, migration, and invasion of HCC cells, whereas upregulation of circ_0001459 had the opposite effect. Moreover, bioinformatics analysis, dual-luciferase reporter assay, RNA immunoprecipitation, and fluorescence in situ hybridization assays were used to predict and verify the interaction between circ_0001459, miR-6165, and the target gene IGF1R. Downregulation of circ_0001459 decreased IGF1R expression and inhibited epithelialto-mesenchymal transition, which could be rescued by treatment with a miR-6165 inhibitor. Mechanistically, we revealed that circ_0001459 could sponge miR-6165 and induce the upregulation of its downstream target IGF1R, thus significantly promoting the progression of HCC. Therefore, circ_0001459 could be a new potential therapeutic target for HCC patients.

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Section: Discussionmentioning

confidence: 99%

“… 27 IGF1R increases the proliferation and glycolysis of pancreatic cancer. 28 HOXB13 accelerates gastric cancer cell migration and invasion by upregulating the expression of IGF1R. 29 IGF1R is activated through miR‐122 downregulation, resulting in activation of the RAS/RAF/ERK pathway in HCC.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA circ_0001459 accelerates hepatocellular carcinoma progression via the miR‐6165/IGF1R axis

Shen

Zhao

Zeng

et al. 2022

Annals of the New York Academy of Sciences

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“…Caveolin-1 (CAV-1) plays an important role in regulating lipid metabolism. Hu et al [ 163 ] revealed that CAV-1 levels in tumor grafts are correlated with the expression levels of the enzymes that regulate lipolysis. TGF-β deficiency can increase stromal autophagy and the generation of ketone bodies.…”

Section: Tgf-β-dependent Metabolism Of Stromal–epithelial Coupling An...mentioning

confidence: 99%

TGF-β signaling in the tumor metabolic microenvironment and targeted therapies

et al. 2022

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Transforming growth factor-β (TGF-β) signaling has a paradoxical role in cancer progression, and it acts as a tumor suppressor in the early stages but a tumor promoter in the late stages of cancer. Once cancer cells are generated, TGF-β signaling is responsible for the orchestration of the immunosuppressive tumor microenvironment (TME) and supports cancer growth, invasion, metastasis, recurrence, and therapy resistance. These progressive behaviors are driven by an “engine” of the metabolic reprogramming in cancer. Recent studies have revealed that TGF-β signaling regulates cancer metabolic reprogramming and is a metabolic driver in the tumor metabolic microenvironment (TMME). Intriguingly, TGF-β ligands act as an “endocrine” cytokine and influence host metabolism. Therefore, having insight into the role of TGF-β signaling in the TMME is instrumental for acknowledging its wide range of effects and designing new cancer treatment strategies. Herein, we try to illustrate the concise definition of TMME based on the published literature. Then, we review the metabolic reprogramming in the TMME and elaborate on the contribution of TGF-β to metabolic rewiring at the cellular (intracellular), tissular (intercellular), and organismal (cancer-host) levels. Furthermore, we propose three potential applications of targeting TGF-β-dependent mechanism reprogramming, paving the way for TGF-β-related antitumor therapy from the perspective of metabolism.

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“…84–86 Table 2 summarizes the mechanism of cachexia. 13,14,34,87–124 The broad picture of CC is summarized in Figure 1.…”

Section: Imbalance Of Anabolism and Catabolism: Insight Into The Mole...mentioning

confidence: 99%

Tumor cell anabolism and host tissue catabolism-energetic inefficiency during cancer cachexia

Hegde

Daimary

Girisa

et al. 2022

Exp Biol Med (Maywood)

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Cancer-associated cachexia (CC) is a pathological condition characterized by sarcopenia, adipose tissue depletion, and progressive weight loss. CC is driven by multiple factors such as anorexia, excessive catabolism, elevated energy expenditure by growing tumor mass, and inflammatory mediators released by cancer cells and surrounding tissues. In addition, endocrine system, systemic metabolism, and central nervous system (CNS) perturbations in combination with cachexia mediators elicit exponential elevation in catabolism and reduced anabolism in skeletal muscle, adipose tissue, and cardiac muscle. At the molecular level, mechanisms of CC include inflammation, reduced protein synthesis, and lipogenesis, elevated proteolysis and lipolysis along with aggravated toxicity and complications of chemotherapy. Furthermore, CC is remarkably associated with intolerance to anti-neoplastic therapy, poor prognosis, and increased mortality with no established standard therapy. In this context, we discuss the spatio-temporal changes occurring in the various stages of CC and highlight the imbalance of host metabolism. We provide how multiple factors such as proteasomal pathways, inflammatory mediators, lipid and protein catabolism, glucocorticoids, and in-depth mechanisms of interplay between inflammatory molecules and CNS can trigger and amplify the cachectic processes. Finally, we highlight current diagnostic approaches and promising therapeutic interventions for CC.

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Caveolin‐1 increases glycolysis in pancreatic cancer cells and triggers cachectic states

Cited by 19 publications

References 40 publications

Circular RNA circ_0001459 accelerates hepatocellular carcinoma progression via the miR‐6165/IGF1R axis

Circular RNA circ_0001459 accelerates hepatocellular carcinoma progression via the miR‐6165/IGF1R axis

TGF-β signaling in the tumor metabolic microenvironment and targeted therapies

Tumor cell anabolism and host tissue catabolism-energetic inefficiency during cancer cachexia

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