HPIP protooncogene differentially regulates metabolic adaptation and cell fate in breast cancer cells under glucose stress via AMPK and RNF2 dependent pathways

Penugurti, Vasudevarao; Khumukcham, Saratchandra Singh; Padala, Chiranjeevi; Dwivedi, Anju; Kamireddy, Karthik Reddy; Srinivasulu, Mukta; Bhopal, Triveni; Manavathi, Bramanandam

doi:10.1016/j.canlet.2021.07.027

Cited by 16 publications

(10 citation statements)

References 71 publications

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“…[ 26 ] Moreover, under chronic glucose stress conditions, RNF2 degrades HRIP via the ubiquitin proteasome pathway leading to apoptosis in breast cancer cells. [ 6 ] In present study, we found that RNF2 was highly expressed in HCC and was associated with malignant clinical features and poor prognosis (Fig. 1 ).…”

Section: Discussionsupporting

confidence: 50%

“…RNF2 is highly expressed in multiple cancer types and contribute to tumor proliferation, metastasis, and drug resistance. [ 6 – 8 ] Wang et al reported that RNF2 could catalyze the mono-ubiquitination of histone H2A at lysine 119 (H2AK119ub). [ 9 ] Meanwhile, previous works revealed a complex “cross-talks” between histone ubiquitination and methylation.…”

Section: Introductionmentioning

confidence: 99%

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RNF2 inhibits E-Cadherin transcription to promote hepatocellular carcinoma metastasis via inducing histone mono-ubiquitination

Yao

Jiang

et al. 2023

Cell Death Dis

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RNF2 is a RING domain-containing E3 ubiquitin ligase that mediate histone H2A mono-ubiquitination to repress gene transcription, but its expression patterns and molecular function in hepatocellular carcinoma (HCC) remain unclear. Herein, we extracted data from TGCA database and validated RNF2 expression in our own cohort, which revealed that RNF2 was highly expressed in HCC and was associated with malignant characteristics and poor prognosis of HCC. Moreover, RNF2 was demonstrated to promote HCC metastasis via enhancing epithelial-mesenchymal transition (EMT) both in vitro and in vivo. Mechanistically, RNF2 repressed E-Cadherin transcription by increasing the deposition of H2K119ub at the E-Cadherin promoter region. In addition, RNF2-regulated crosstalk between H2AK119ub, H3K27me3 and H3K4me3 synergistically reduced E-Cadherin transcription, which promoted EMT and HCC metastasis. These results indicate that RNF2 played an oncogenic role in HCC progression via inducing EMT, and RNF2 could be a potential therapeutic target for HCC.

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Section: Discussionsupporting

confidence: 50%

Section: Introductionmentioning

confidence: 99%

RNF2 inhibits E-Cadherin transcription to promote hepatocellular carcinoma metastasis via inducing histone mono-ubiquitination

Yao

Jiang

et al. 2023

Cell Death Dis

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“…FOXO3a is promoted by glucose stress-induced AMPK activation and FOXO3a dramatically upregulates hematopoietic PBX1-interacting protein (HPIP) to increase glutamine uptake in response to glucose stress. Interestingly, prolonged glucose stress leads to degradation of HPIP, leading to cell death in order [ 125 ]. AMPK activation reprograms folate cycle metabolism, related to the feature of purine biosynthesis, which is restrained by the proliferator-activated receptor γ co-activator 1α (PGC-1α)/estrogen-related receptor α (ERRα) axis [ 126 ].…”

Section: Pleiotropic Regulations Of Ampk In Breast Cancermentioning

confidence: 99%

Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer

et al. 2023

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Breast cancer is a common cancer in women worldwide. The existing clinical treatment strategies have been able to limit the progression of breast cancer and cancer metastasis, but abnormal metabolism, immunosuppression, and multidrug resistance involving multiple regulators remain the major challenges for the treatment of breast cancer. Adenosine 5′-monophosphate (AMP)-Activated Protein Kinase (AMPK) can regulate metabolic reprogramming and reverse the “Warburg effect” via multiple metabolic signaling pathways in breast cancer. Previous studies suggest that the activation of AMPK suppresses the growth and metastasis of breast cancer cells, as well as stimulating the responses of immune cells. However, some other reports claim that the development and poor prognosis of breast cancer are related to the overexpression and aberrant activation of AMPK. Thus, the role of AMPK in the progression of breast cancer is still controversial. In this review, we summarize the current understanding of AMPK, particularly the comprehensive bidirectional functions of AMPK in cancer progression; discuss the pharmacological activators of AMPK and some specific molecules, including the natural products (including berberine, curcumin, (−)-epigallocatechin-3-gallate, ginsenosides, and paclitaxel) that influence the efficacy of these activators in cancer therapy; and elaborate the role of AMPK as a potential therapeutic target for the treatment of breast cancer.

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“…It is an energy-sensitive molecule and is activated under conditions of cellular stress, a common phenomenon in cancer cells. However, a few reports argue this activation may actually protect cancer cells [41]; nevertheless, there is ample evidence to suggest the therapeutic action of AMPK activation on cancer stem cells, particularly breast cancer stem cells [31,[42][43][44][45][46][47]. Paclitaxel, a well-known and commonly used drug for the treatment of breast and lung cancers, involves the activation of AMPK during its therapeutic pathway [48].…”

Section: Ampk Activation For the Treatment Of Breast Cancer Stem Cellsmentioning

confidence: 99%

Targeting Breast Cancer and Their Stem Cell Population through AMPK Activation: Novel Insights

Uprety

Abrahamse

2022

Cells

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Despite some significant advancements, breast cancer has become the most prevalent cancer in the world. One of the main reasons for failure in treatment and metastasis has been attributed to the presence of cancer initiating cells—cancer stem cells. Consequently, research is now being focussed on targeting cancer cells along with their stem cell population. Non-oncology drugs are gaining increasing attention for their potent anticancer activities. Metformin, a drug commonly used to treat type 2 diabetes, is the best example in this regard. It exerts its therapeutic action by activating 5′ adenosine monophosphate-activated protein kinase (AMPK). Activated AMPK subsequently phosphorylates and targets several cellular pathways involved in cell growth and proliferation and the maintenance of stem-like properties of cancer stem cells. Therefore, AMPK is emerging as a target of choice for developing effective anticancer drugs. Vanadium compounds are well-known PTP inhibitors and AMPK activators. They find extensive applications in treatment of diabetes and obesity via PTP1B inhibition and AMPK-mediated inhibition of adipogenesis. However, their role in targeting cancer stem cells has not been explored yet. This review is an attempt to establish the applications of insulin mimetic vanadium compounds for the treatment of breast cancer by AMPK activation and PTP1B inhibition pathways.

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HPIP protooncogene differentially regulates metabolic adaptation and cell fate in breast cancer cells under glucose stress via AMPK and RNF2 dependent pathways

Cited by 16 publications

References 71 publications

RNF2 inhibits E-Cadherin transcription to promote hepatocellular carcinoma metastasis via inducing histone mono-ubiquitination

RNF2 inhibits E-Cadherin transcription to promote hepatocellular carcinoma metastasis via inducing histone mono-ubiquitination

Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer

Targeting Breast Cancer and Their Stem Cell Population through AMPK Activation: Novel Insights

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