miR-122 Targets Pyruvate Kinase M2 and Affects Metabolism of Hepatocellular Carcinoma

Liu, Angela M.; Xu, Zhi; Shek, Felix H.; Wong, Kwong-Fai; Lee, Nikki P.; Poon, Ronnie T. P.; Chen, Jinfei; Luk, John M.

doi:10.1371/journal.pone.0086872

Cited by 112 publications

(91 citation statements)

References 25 publications

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“…Moreover, miR-122 is a negative regulator of PKM2 by directly interacting with the 3′-untranslated region of the latter [56]. Similar findings were reported by Liu et al [57]. As a crucial regulator of HCC glycolysis, several key modulators of PKM2 have been identified in recent years.…”

Section: Hcc and Cancer Metabolismsupporting

confidence: 84%

Molecular Pathogenesis of Hepatocellular Carcinoma

Ho¹,

Lo²,

Chan³

et al. 2016

Liver Cancer

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The pathogenesis of hepatocellular carcinoma (HCC) is a multistep process involving the progressive accumulation of molecular alterations pinpointing different molecular and cellular events. The next-generation sequencing technology is facilitating the global and systematic evaluation of molecular landscapes in HCC. There is emerging evidence supporting the importance of cancer metabolism and tumor microenvironment in providing a favorable and supportive niche to expedite HCC development. Moreover, recent studies have identified distinct surface markers of cancer stem cell (CSC) in HCC, and they also put forward the profound involvement of altered signaling pathways and epigenetic modifications in CSCs, in addition to the concomitant drug resistance and metastasis. Taken together, multiple key genetic and non-genetic factors, as well as liver CSCs, result in the development and progression of HCC.

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Section: Hcc and Cancer Metabolismsupporting

confidence: 84%

Molecular Pathogenesis of Hepatocellular Carcinoma

Ho¹,

Lo²,

Chan³

et al. 2016

Liver Cancer

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“…There was no significant difference for PKM2 mRNA in the breast cancer with miR-122-5p or the miRNA control transfection, but, PKM2 protein showed down-regulation in the cells. HK2 was regulated by miR-143 [24], miR-155 [25], miR-199a-5p [26], miR-29b [27,[28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43], miR-140-5p in various cancers like bladder cancer, liver cancer and prostate cancer. LDHA was regulated by miR-383, miR34a, miR-122, miR-30a-5p and other miRNAs in cancer.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

Xia¹,

Yu²,

Mao³

et al. 2018

Oncotarget

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Exosomes contain many important components including miRNAs for cancerstromal communication. Mesenchymal stromal cells support tumor development, however, the low expression of miRNAs in exosomes and their regulation roles from mesenchymal stromal cells are still unclear. In this study, we hypothesized that mesenchymal stromal cells-derived exosomes promote breast cancer cell glycolysis. Our results showed that mesenchymal stromal cells-derived exosomes promoted cell proliferation and glycolysis of breast cancer cells. Furthermore, sequencing of exosomal RNAs revealed miR-216b-5p, miR-33a-5p and miR-122-5p were lack of expression in exosomes from mesenchymal stromal cells. MiR-216b-5p, miR-33a-5p and miR-122-5p overexpression in breast cancer cells suppressed glycolysis by targeting HK2, LDHA and PKM2 respectively. These results provided valuable insights and mechanism of mesenchymal stromal cells-secreted exosomes on the glycolysis of breast cancer.

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“…For instances, pyruvate kinase type M (PKM) may be associated with the effect of OA on lung cancer cells. PKM has been shown as a confirmed target of miR-122 in liver cancer cells [18]. Furthermore, OA has been verified to regulate PKM function and suppress the proliferation of cancer cells [3].…”

Section: Discussionmentioning

confidence: 96%

Oleanolic acid suppresses the proliferation of lung carcinoma cells by miR-122/Cyclin G1/MEF2D axis

Zhao

Liu

2014

Mol Cell Biochem

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Oleanolic acid (OA) is a natural compound from plants with anti-tumor activities. However, the mechanism of the inhibitory effect of OA on cell cycle progression has not been completely explored. We employed several lung carcinoma cell lines to investigate the cell cycle-related molecular pathway affected by OA. The data revealed that OA suppressed the proliferation of lung cancer cells in both dose- and time-dependent manners, along with an increase in miR-122 abundance. The suppression of miR-122 abolished the effect of OA on lung cancer cells. CCNG1 and MEF2D, two putative miR-122 targets, were found to be downregulated by OA treatment. Restoring their expression counteracted the effect of OA on lung carcinoma cells. OA was further shown to induce the expression of miR-122-regulating transcriptional factors in lung cancer cells. Collectively, OA induced cell cycle arrest in lung cancer cells through miR-122/Cyclin G1/MEF2D pathway. This finding may contribute to the understanding of the molecular mechanism of OA's anti-tumor activity.

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miR-122 Targets Pyruvate Kinase M2 and Affects Metabolism of Hepatocellular Carcinoma

Cited by 112 publications

References 25 publications

Molecular Pathogenesis of Hepatocellular Carcinoma

Molecular Pathogenesis of Hepatocellular Carcinoma

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

Oleanolic acid suppresses the proliferation of lung carcinoma cells by miR-122/Cyclin G1/MEF2D axis

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