SIRT2 Promotes the Migration and Invasion of Gastric Cancer through RAS/ERK/JNK/MMP-9 Pathway by Increasing PEPCK1-Related Metabolism

Yang, Li; Zhang, Mingming; Dorfman, Robert; Pan, Yida; Tang, Dehua; Xu, Lei; Zhao, Zhenguo; Zhou, Qian; Zhou, Lixing; Wang, Yuming; Yin, Yuyao; Shen, Shanshan; Kong, Bo; Frieß, Helmut; Zhao, Shimin; Wang, Lei; Zou, Xiaoping

doi:10.1016/j.neo.2018.03.008

Cited by 81 publications

(96 citation statements)

References 55 publications

(86 reference statements)

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“…Apoptosis NSCLC [40] P53 CCA [41] MYC Metastasis HCC [42,43] AKT/GSK3β/β-catenin Axis GC [44] Tumorigenesis BC [45] Slug HCC [39] APC, CDC20 BC [39] APC, CDC20 SIRT3 Viability BLC [46] P53 PC [47] MYC; PI3K/AKT pathway CRC [48] AKT/PTEN NSCLC [49] Bax/Bcl-2, P53 HCC [50] PI3K/AKT pathway PDC [51] Apoptosis NSCLC [49] Bax/Bcl-2, P53 OSCC [52] RIP Leukemia [53] AKT, Bax/Bcl-2 Metastasis CRC [48] AKT/PTEN HCC [50] PI3K/AKT pathway PDC [51] PC [54] FOXO3A, Wnt/β-catenin pathway OC [55] Twist [57] ERK/Drp1 Axis ESCC [58] GDH CRC [59] GC [60] Apoptosis Metastasis NSCLC [57] ERK/Drp1 Axis ESCC [58] GDH CRC [59] E-cadherin GC [60] E-cadherin [72] COX-2, AKT, AMPK CRC [73] PTEN/AKT signaling ACC [74] NF-κB signaling GBM [75] JAK2/STAT3 pathway Apoptosis CRC [73] PTEN/AKT signaling HCC [70] Bax GBM [75] AK2/STAT3 pathway FSA [76] NF-κB signaling HCC [77,78] ERK1/2 pathway CC [76] NF-κB signaling Metastasis HCC [71,79] PKM2 CRC…”

Section: Sirtuins and Viability In Cancersmentioning

confidence: 99%

The Roles of Sirtuin Family Proteins in Cancer Progression

Zhao

Hou

et al. 2019

Cancers

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Sirtuin family members are characterized by either mono-ADP-ribosyltransferase or deacylase activity and are linked to various cancer-related biological pathways as regulators of transcriptional progression. Sirtuins play fundamental roles in carcinogenesis and maintenance of the malignant phenotype, mainly participating in cancer cell viability, apoptosis, metastasis, and tumorigenesis. Although sirtuin family members have a high degree of homology, they may play different roles in various kinds of cancer. This review highlights their fundamental roles in tumorigenesis and cancer development and provides a critical discussion of their dual roles in cancer, namely, as tumor promoters or tumor suppressors.

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Section: Sirtuins and Viability In Cancersmentioning

confidence: 99%

The Roles of Sirtuin Family Proteins in Cancer Progression

Zhao

Hou

et al. 2019

Cancers

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“…Recently, SIRT2 was found to be associated with mitotic cell cycle control [11][12][13], in which SIRT2 likely promoted tumorigenesis [14][15][16][17]. Upregulation of SIRT2 has been detected in a number of tumors [16][17][18][19][20][21][22]. However, it is not known whether SIRT2 is a CSC marker in cancers, including RCC.…”

Section: Introductionmentioning

confidence: 99%

Role of SIRT2 in Regulation of Stemness of Cancer Stem-Like Cells in Renal Cell Carcinoma

Wei¹,

He²,

Zhang³

2018

Cell Physiol Biochem

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Background/Aims: Cancer stem cells (CSCs) contribute to tumorgenesis, invasion and metastasis, and are typically resistant to chemotherapy. Recent reports showed that SIRT2 was upregulated in several cancers. However, whether SIRT2 may be a CSC marker in renal cell carcinoma (RCC) is not clear. Methods: The SIRT2 levels in both RCC samples and the corresponding normal kidney samples (NT) were assessed by RT-qPCR and ELISA. The association between SIRT2 levels and patient survival was examined using Bivariate correlation analysis by Spearman’s Rank Correlation Coefficients. The survival of the patients was analyzed using Kaplan-Meier curve. In vitro, 2 RCC cell lines were co-transduced with a lentivirus expressing both a green fluorescent protein and a luciferase reporter under a cytomegalovirus promoter, and another lentivirus expressing a nuclear red fluorescent protein reporter under the control of a SIRT2 promoter for differentiating SIRT2+ vs SIRT2- RCC cells by flow cytometry. The SIRT2+ vs SIRT2- RCC cells were examined for the potential of forming tumor sphere in a tumor sphere formation assay, resistance to fluorouracil-induced apoptosis by CCK-8 assay, and the frequency of forming tumor in vivo after serial adoptive transplantation by bioluminescence. Results: The levels of SIRT2 were higher in RCC samples than NT. The prognosis of RCC patients with high SIRT2 was worse than that of with low SIRT2. Compared to SIRT2- cells, SIRT2+ cells formed more tumor spheres, appeared to be more resistant towards fluorouracil-induced apoptosis, and generated bigger tumors with higher frequency after serial adoptive transplantation. Conclusion: SIRT2 may be highly expressed in the RCC stem-like cells and regulates cancer metastasis. Selective knockout of SIRT2 or elimination of SIRT2+ cells may improve the therapeutic outcome for patients with RCC.

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“…Noticeably, HDAC2 could bind to different loci on chromosome 11 and can modulate MMP27 bidirectionally. Previous studies suggested that the HDAC family could regulate multiple MMPs, including MMP1, MMP2, MMP3, MMP7, MMP9, MMP10, MMP13, MMP14, and MMP28, 23‐28 and that MMP10 could be regulated by HDAC3 and HDAC7 28,29 . For the first time, we found that HDAC2 could potentially modulate the MMP10, MMP16, MMP21, MMP25‐AS1, MMP27, and CD16 genes in neutrophils of AIS patients.…”

Section: Discussionmentioning

confidence: 55%

Intravenous antagomiR‐494 lessens brain‐infiltrating neutrophils by increasing HDAC2‐mediated repression of multiple MMPs in experimental stroke

Zhao

et al. 2020

FASEB j.

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Neutrophil infiltration and phenotypic transformation are believed to contribute to neuronal damage in ischemic stroke. Emerging evidence suggests that histone deacetylase 2 (HDAC2) is an epigenetic regulator of inflammatory cells. Here, we aimed to investigate whether microRNA-494 (miR-494) affects HDAC2-mediated neutrophil infiltration and phenotypic shift. MiR-494 levels in neutrophils from acute ischemic stroke (AIS) patients were detected by real-time PCR. Chromatin Immunoprecipitation (ChIP)-Seq was performed to clarify which genes are the binding targets of HDAC2. Endothelial cells and cortical neurons were subjected to oxygen-glucose deprivation (OGD), transwell assay was conducted to examine neutrophil migration through endothelial cells, and neuronal injury was examined after stimulating with supernatant from antagomiR-494-treated neutrophils. C57BL/6J mice were subjected to transient middle cerebral artery occlusion (MCAO) and an-tagomiR-494 was injected through tail vein immediately after reperfusion, and neutrophil infiltration and phenotypic shift was examined. We found that the expression of miR-494 in neutrophils was significantly increased in AIS patients. HDAC2 targeted multiple matrix metalloproteinases (MMPs) and Fc-gamma receptor III (CD16) genes in neutrophils of AIS patients. Furthermore, antagomiR-494 repressed expression of multiple MMPs genes, including MMP7, MMP10, MMP13, and MMP16, which reduced the number of brain-infiltrating neutrophils by regulating HDAC2.AntagomiR-494 could also exert its neuroprotective role through inhibiting the shift of neutrophils toward pro-inflammatory N1 phenotype in vivo and in vitro. Taken together, miR-494 may serve as an alternative predictive biomarker of the outcome

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SIRT2 Promotes the Migration and Invasion of Gastric Cancer through RAS/ERK/JNK/MMP-9 Pathway by Increasing PEPCK1-Related Metabolism

Cited by 81 publications

References 55 publications

The Roles of Sirtuin Family Proteins in Cancer Progression

The Roles of Sirtuin Family Proteins in Cancer Progression

Role of SIRT2 in Regulation of Stemness of Cancer Stem-Like Cells in Renal Cell Carcinoma

Intravenous antagomiR‐494 lessens brain‐infiltrating neutrophils by increasing HDAC2‐mediated repression of multiple MMPs in experimental stroke

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