AMPKα2 knockout enhances tumour inflammation through exacerbated liver injury and energy deprivation‐associated AMPKα1 activation

Qiu, Siqi; Liu, Taoyan; Piao, Chunmei; Wang, Ying; Wang, Kefang; Zhou, Yandong; Cai, Liang; Zheng, Shuai; Lan, Feng; Du, Jie

doi:10.1111/jcmm.13978

Cited by 11 publications

(10 citation statements)

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“…found that AMPK activation inhibited tumor metastasis. [ 103 ] In the liver metastasis model of colon cancer cells, AMPKα2 knockout attenuated liver damage and inflammation. AMPKα2 knockout decreased the total amount of AMPK, and there was no obvious compensation for AMPKα1, although AMPKα1 was still appeared in the liver tissue of tumor metastasis.…”

Section: The Relationship Between Ampk Activation and Carcinogenesismentioning

confidence: 99%

“…AMPKα2 knockout decreased the total amount of AMPK, and there was no obvious compensation for AMPKα1, although AMPKα1 was still appeared in the liver tissue of tumor metastasis. [ 103 ] In the AOM and DSS mouse model, AOM‐DSS treatment cause colitis and colonic cancer. AMPK activator metformin significantly inhibited the growth of colon polyps, which are one of the important factors to lead carcinogenesis.…”

Section: The Relationship Between Ampk Activation and Carcinogenesismentioning

confidence: 99%

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Targeting AMPK Signaling by Dietary Polyphenols in Cancer Prevention

Cao

et al. 2021

Molecular Nutrition Food Res

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Cancer is a serious public health problem in the world and a major disease affecting human health. Dietary polyphenols have shown good potential in the treatment of various cancers. It is worth noting that cancer cells usually exhibit metabolic abnormalities of high glucose intake and inefficient utilization. AMPK is the key molecule in the regulation of energy metabolism and is closely related with obesity and diabetes. Recent studies indicate that AMPK also plays an important role in cancer prevention and regulating cancer‐related genes and pathways, and dietary polyphenols can significantly regulate AMPK activity. In this review, the progress of dietary polyphenols preventing carcinogenesis via AMPK pathway is systemically summarized. From the viewpoint of interfering energy metabolism, the anti‐cancer effects of dietary polyphenols are explained. AMPK pathway modulated by different dietary polyphenols affects pathways and target genes are summarized. Dietary polyphenols exert anti‐cancer effect through the target molecules regulated by AMPK, which broadens the understanding of polyphenols anti‐cancer mechanisms and provides value reference for the investigators of the novel field.

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Section: The Relationship Between Ampk Activation and Carcinogenesismentioning

confidence: 99%

Section: The Relationship Between Ampk Activation and Carcinogenesismentioning

confidence: 99%

Targeting AMPK Signaling by Dietary Polyphenols in Cancer Prevention

Cao

et al. 2021

Molecular Nutrition Food Res

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“…28 In liver cancer, PRKAA2 knockout enhanced tumor inflammation. 29 In addition, PRKAA2 has been shown to act as a tumor repressor in CRC. 30,31 As a subunit of AMPK, PRKAA2 has been shown to inhibit cell proliferation through the p53/p21 pathway, and through modulation of the expression of p27.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-4999-5p Predicts Colorectal Cancer Survival Outcome and Reprograms Glucose Metabolism by Targeting PRKAA2</p>

Zhang¹,

Huang²,

Zhu³

et al. 2020

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Purpose: Colorectal cancer (CRC) is the third most common cancer, and the second leading cause of cancer death worldwide. Dysregulation of microRNAs has been shown to modulate glucose metabolic reprogramming in CRC. However, the functional role of miR-4999-5p in the CRC glucose metabolic shift has not been characterized. Patients and Methods: The levels of miR-4999-5p and PRKAA2 were evaluated by RT-qPCR. Univariate and multivariate survival analyses were conducted to evaluate the prognostic value of miR-4999-5p. Cell proliferation was assessed using the CCK-8 and colony formation assays. Extracellular acidification rate, glucose uptake, cellular glucose-6-phosphate level, and lactate production were evaluated to assess the effects of miR-4999-5p on CRC glycolysis. Dual-luciferase reporter assay was conducted to investigate the direct interaction between miR-4999-5p and PRKAA2. Mouse xenograft models were established to assess the functions of miR-4999-5p in vivo. Results: miR-4999-5p was highly expressed in CRC tissues and cell lines. In addition, miR-4999-5p was associated with tumor differentiation and TNM stage, and elevated expression of miR-4999-5p was an independent predictor of poorer overall survival. Furthermore, miR-4999-5p promoted cell proliferation and glycolysis in CRC. miR-4999-5p targeted PRKAA2 to exert its tumor-promoting functions, and PRKAA2 knockdown rescued decreased cell proliferation and glycolysis in miR-4999-5p-silenced CRC cells. In vivo experiments showed that miR-4999-5p promoted CRC growth. Conclusion: miR-4999-5p facilitated cell growth and glucose metabolic reprogramming through direct targeting of PRKAA2. Our results showed that miR-4999-5p may be a novel prognostic marker and therapeutic target for CRC.

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“…Targeting specific components or activities of mitochondria such as Complex I assembly, the electron transport chain (ETC), mitochondrial fission rates, the process of biogenesis, mitochondrial sirtuin molecules and/or disruption of the TCA cycle can trigger, or sometimes, prevent senescence [46,[54][55][56][57]. Further, modulation of the AMP:ATP or ADP:ATP ratio during senescence consolidates cell-cycle arrest by activating AMP-activated protein kinase (AMPK), a cytoplasmic sensor that detects environmental or nutritional stress and maintains energy balance [52,58].…”

Section: Mitochondrial Alterationsmentioning

confidence: 99%