TRPM3 and miR-204 Establish a Regulatory Circuit that Controls Oncogenic Autophagy in Clear Cell Renal Cell Carcinoma

Hall, Daniel; Cost, Nicholas G.; Hegde, Shailaja; Kellner, Emily; Mikhaylova, Olga; Stratton, Yiwen; Ehmer, Birgit; Abplanalp, William; Pandey, Raghav; Biesiada, Jacek; Harteneck, Christian; Plas, David R.; Meller, Jarosław; Czyzyk-Krzeska, Maria F.

doi:10.1016/j.ccell.2014.09.015

Cited by 156 publications

(172 citation statements)

References 58 publications

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“…Interestingly, TRPM3 was validated to be a target of miR-204 [51], consistent with that some genes are autoregulated via intronic microRNAs [73]. Some stimuli may induce expression of both miR-204 and TRPM3 .…”

Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 80%

“…Therefore, both TRPM3 and miR-204 can play their roles only temporarily in these circumstances. With the role of TRPM3 in cancers [51, 74], the TRPM3-miR-204 feedback loop may be important to prevent progression of oncogenic transformation and may also exist widely in physiological situations.…”

Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 99%

“…TRPM3 is overexpressed in choroid plexus papillomas, glioblastoma multiforme, and clear cell renal cellcarcinoma (ccRCC) [51, 74], suggesting that TRPM3 has a tumor-promoting role. It is currently unknown whether miR-204 expression actually increases as a result of TRPM3 overexpression in choroid plexus papillomas and glioblastoma multiforme.…”

Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 99%

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The dual regulatory role of miR-204 in cancer

Pan

2016

Tumor Biol.

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MicroRNAs (miRNAs) are a group of endogenous, small (about 22 nucleotides) non-coding RNAs which negatively regulate gene expressions. As one of them, miR-204 originates from the sixth intron of the transient receptor potential melastatin 3 (TRPM3) gene. Therefore, expression of miR-204 is under the control of the TRPM3 promoter and regulated by genetic and epigenetic mechanisms. miR-204 has been found to play the important roles in development of eyes and adipogenesis. Its pathological functions have been observed in a few diseases including pulmonary arterial hypertension, diabetes, and various types of cancers. It is believed that miR-204 acts as a tumor-suppressor via promoting apoptosis, conferring the resistance of cancer cells to chemotherapy, and suppressing the self-renewal of cancer stem cells (CSCs) and the epithelial to mesenchymal transition (EMT). Expression of miR-204 is repressed by its targets XRN1 and TRKB in prostate cancer and endometrial carcinoma, respectively; therefore, they establish an oncogenic feedback loops that play an important role promoting development of cancer. In this review, we summarize our current knowledge regarding miR-204, including its expression, regulation and biological functions, especially focusing our discussion on its role in tumor development and tumor progression.

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Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 80%

Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 99%

Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 99%

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The dual regulatory role of miR-204 in cancer

Pan

2016

Tumor Biol.

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“…Finally, in renal carcinoma, the influx of Ca 21 and zinc through the TRPM3 channel in the plasma membrane, respectively, activates the CaMKK2-AMPK pathway and suppresses the increase of miR-241, a microRNA that targets LC3, thus stimulating autophagy. In this model, autophagy contributes to tumor growth (Hall et al, 2014). These varied outcomes may be attributed to: 1) the presence or absence and the levels of key proteins involved in the connection between Despite not being assessed, in these contexts, autophagy is known to be cytoprotective (Lum et al, 2005;Onodera and Ohsumi, 2005).…”

Section: Autophagy Ca 21 and Cancermentioning

confidence: 99%

Modulation of Autophagy by Calcium Signalosome in Human Disease

et al. 2016

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Autophagy is a catabolic process that is largely regulated by extracellular and intracellular signaling pathways that are central to cellular metabolism and growth. Mounting evidence has shown that ion channels and transporters are important for basal autophagy functioning and influence autophagy to handle stressful situations. Besides its role in cell proliferation and apoptosis, intracellular Ca 21 is widely recognized as a key regulator of autophagy, acting through the modulation of pathways such as the mechanistic target of rapamycin complex 1, calcium/calmodulin-dependent protein kinase kinase 2, and protein kinase C. Proper spatiotemporal Ca 21 availability, coupled with a controlled ionic flow among the extracellular milieu, storage compartments, and the cytosol, is critical in determining the role played by Ca 21 on autophagy and on cell fate. The crosstalk between Ca 21 and autophagy has a central role in cellular homeostasis and survival during several physiologic and pathologic conditions. Here we review the main findings concerning the mechanisms and roles of Ca 21 -modulated autophagy, focusing on human disorders ranging from cancer to neurologic diseases and immunity. By identifying mechanisms, players, and pathways that either induce or suppress autophagy, new promising approaches for preventing and treating human disorders emerge, including those based on the modulation of Ca 21 -mediated autophagy.

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“…Inhibition of TRPC6 expression in human renal adenocarcinoma ACHN cells suppressed proliferation and prolonged RCC cells G2/M phase transition, suggesting TRPC6 channel as a key regulator of RCC development (Song et al, 2013). Also TRPM3 has been shown to play a role in RCC development, promoting growth of clear cell renal cell carcinoma (ccRCC) and stimulating autophagy MAP1LC3A (LC3A) and MAP1LC3B (LC3B) (Hall et al, 2014).…”

Section: Trp Expression In Cancermentioning

confidence: 99%

Human transient receptor potential (TRP) channel expression profiling in carcinogenesis

Bernardini¹,

Fiorio²,

Prevarskaya³

et al. 2015

Int. J. Dev. Biol.

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Despite the intensive research of the last three decades into Transient Receptor Potential (TRP) cation channels, no precise and complete profiling of these channels is yet available regarding their involvement in physiopathology and carcinogenesis in particular. TRP channel activity is crucial for all the essential hallmarks of carcinogenesis such as proliferation, apoptosis, migration and angiogenesis, which is the reason why these channels have been proposed not only as clinical markers, but also as promising targets for anti-cancer therapy. However, in the majority of studies, each channel has been considered as a separate molecular entity and studied independently from the other TRPs, while a complete "transportome" of the specific stages of carcinogenesis is required for the effective use of these targets. This review focuses on the partial TRP expression profiles found in the literature and the means by which a full TRP signature could be achieved.

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TRPM3 and miR-204 Establish a Regulatory Circuit that Controls Oncogenic Autophagy in Clear Cell Renal Cell Carcinoma

Cited by 156 publications

References 58 publications

The dual regulatory role of miR-204 in cancer

The dual regulatory role of miR-204 in cancer

Modulation of Autophagy by Calcium Signalosome in Human Disease

Human transient receptor potential (TRP) channel expression profiling in carcinogenesis

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