Caveolin-1 in the regulation of cell metabolism: a cancer perspective

Nwosu, Zeribe C.; Ebert, Matthias; Dooley, Steven; Meyer, Christoph

doi:10.1186/s12943-016-0558-7

Cited by 174 publications

(141 citation statements)

References 116 publications

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“…In line with this study, overexpression of caveolin 1 is shown to increase cholesterol efflux and reduce the proliferation of human skin fibroblasts [51]. However, dysregulation of caveolin 1 expression is found in multiple types of cancer [52,53,54]. It should be clarified in which cellular context caveolin 1 functions as a tumor suppressor or an oncogene and whether altered intracellular cholesterol levels by caveolin 1 could suppress or promote cancer progression.…”

Section: Regulation Of Lipid Metabolism By Wild-type P53mentioning

confidence: 56%

p53 as a Regulator of Lipid Metabolism in Cancer

Parrales

Iwakuma

2016

IJMS

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Enhanced proliferation and survival are common features of cancer cells. Cancer cells are metabolically reprogrammed which aids in their survival in nutrient-poor environments. Indeed, changes in metabolism of glucose and glutamine are essential for tumor progression. Thus, metabolic reprogramming is now well accepted as a hallmark of cancer. Recent findings suggest that reprogramming of lipid metabolism also occurs in cancer cells, since lipids are used for biosynthesis of membranes, post-translational modifications, second messengers for signal transduction, and as a source of energy during nutrient deprivation. The tumor suppressor p53 is a transcription factor that controls the expression of proteins involved in cell cycle arrest, DNA repair, apoptosis, and senescence. p53 also regulates cellular metabolism, which appears to play a key role in its tumor suppressive activities. In this review article, we summarize non-canonical functions of wild-type and mutant p53 on lipid metabolism and discuss their association with cancer progression.

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Section: Regulation Of Lipid Metabolism By Wild-type P53mentioning

confidence: 56%

p53 as a Regulator of Lipid Metabolism in Cancer

Parrales

Iwakuma

2016

IJMS

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“…In fact, in ours results we demonstrated that GRX EGFP‐Cav1 cells endocytosed more FluorSpheres® when compared with GRX. Importantly, Cav‐1 and its interactions with actin cytoskeleton and ATP play a pivotal role in the structure, formation, and function of caveolae . Although these results may be related to the increase on the caveolae number, it is possible that FluorSpheres® uptake can be being driven by both caveolar endocytosis or clathrin‐dependent endocytosis …”

Section: Discussionmentioning

confidence: 99%

Exogenous expression of caveolin‐1 is sufficient for hepatic stellate cell activation

Ilha

Moraes

Rohden

et al. 2019

J of Cellular Biochemistry

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Caveolin‐1 (Cav‐1) expression is increased in hepatic stellate cells (HSC) upon liver cirrhosis and it functions as an integral membrane protein of lipid rafts and caveolae that regulates and integrates multiple signals as a platform. This study aimed to evaluate the role of Cav‐1 in HSC. Thus, the effects of exogenous expression of Cav‐1 in GRX cells, a model of activated HSC, were determined. Here, we demonstrated through evaluating well‐known HSC activation markers – such as α‐smooth muscle actin, collagen I, and glial fibrillary acidic protein – that up regulation of Cav‐1 induced GRX to a more activated phenotype. GRXEGFP‐Cav1 presented an increased migration, an altered adhesion pattern, a reorganization f‐actin cytoskeleton, an arrested cell cycle, a modified cellular ultrastructure, and a raised endocytic flux. Based on this, GRX EGFP‐Cav1 represents a new cellular model that can be an important tool for understanding of events related to HSC activation. Furthermore, our results reinforce the role of Cav‐1 as a molecular marker of HSC activation.

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“…TP53‐induced glycolysis and apoptosis regulator was further upregulated in the co‐cultured breast cancer cells, which resulted in apoptosis inhibition, and thus supports the hypothesis that stromal CAV1 possesses tumor‐suppressor properties, whereas loss of stromal CAV1 fosters malignant epithelial cell resistance by evading apoptosis . Thus, restoring CAV1 expression in respective stromal cells could inhibit the cancer cell metabolism . Excessive reactive species not only induce oxidative damages and inactivation of tumor suppressor genes but also activate the phosphorylation of CAV1, which was reported to promote cancer cell growth and survival .…”

Section: Introductionmentioning

confidence: 99%

“…Another resistance promoting factor is autophagy, as cancers can upregulate autophagy to survive microenvironmental stress and to increase growth and aggressiveness . CAV1 was already directly associated with autophagy . In CAV1 expressing human breast cancer cells the expression of CAV1 and autophagy‐related proteins were induced and inhibited apoptosis upon Estradiol treatment, a crucial regulator of cell growth by mediating autophagy and apoptosis in breast cancer cells .…”

Section: Introductionmentioning

confidence: 99%

Caveolin‐1, cancer and therapy resistance

Ketteler

Klein

2018

Intl Journal of Cancer

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Resistance of solid tumors to chemo- and radiotherapy remains a major obstacle in anti-cancer treatment. Herein, the membrane protein caveolin-1 (CAV1) came into focus as it is highly expressed in many tumors and high CAV1 levels were correlated with tumor progression, invasion and metastasis, and thus a worse clinical outcome. Increasing evidence further indicates that the heterogeneous tumor microenvironment, also known as the tumor stroma, contributes to therapy resistance resulting in poor clinical outcome. Again, CAV1 seems to play an important role in modulating tumor host interactions by promoting tumor growth, metastasis, therapy resistance and cell survival. However, the mechanisms driving stroma-mediated tumor growth and radiation resistance remain to be clarified. Understanding these interactions and thus, targeting CAV1 may offer a novel strategy for preventing cancer therapy resistance and improving clinical outcomes. In this review, we will summarize the resistance-promoting effects of CAV1 in tumors, and emphasize its role in the tumor-stroma communication as well as the resulting malignant phenotype of epithelial tumors.

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Caveolin-1 in the regulation of cell metabolism: a cancer perspective

Cited by 174 publications

References 116 publications

p53 as a Regulator of Lipid Metabolism in Cancer

p53 as a Regulator of Lipid Metabolism in Cancer

Exogenous expression of caveolin‐1 is sufficient for hepatic stellate cell activation

Caveolin‐1, cancer and therapy resistance

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