<i>Retracted</i>: Silencing of COL1A2, COL6A3, and THBS2 inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the PI3k‐Akt signaling pathway

Ao, Ran; Lin, Guozhen; Wáng, Ying; Wang, Jiani

doi:10.1002/jcb.26524

Cited by 115 publications

(92 citation statements)

References 39 publications

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“…The 43 genes with similar expression patterns are likely to have related functions in the aggressive growth and metastasis of cancers (64). In the PPI network, the genes of AEBP1, MMP14, OLFML2B, PDGFRB, SERPINE1, SPARC, SFRP2, COL1A2, COL6A3, THBS2, COL5A2, COL11A1, FAP, MXRA5 and THY1 were upregulated in solid cancer tissues, and significantly associated with the overall survival of patients with cancer (74)(75)(76)(77)(78)(79)(80)(81)(82). Some genes in the PPI network, including AEBP1, OLFML2B, PDGFRB, SERPINE1, COL1A2, COL6A3, and THBS2 have been reported to be associated with metastasis, invasion and migration in cancer cells (74,76,80,83,84).…”

Section: Discussionmentioning

confidence: 99%

Biglycan as a potential diagnostic and prognostic biomarker in multiple human cancers

Zhao

Yin

Zhao³

et al. 2020

Oncol Lett

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Biglycan (BGN), a key member of the small leucine-rich proteoglycan family, is an important component of the extracellular matrix. Clinical studies have demonstrated that upregulation of BGN is associated with poor prognosis in patients with various types of solid cancer. The present study analyzed the mRNA expression levels of BGN in various types of solid cancer when compared with that in normal tissues via the Oncomine database. The UALCAN, OncoLnc and Kaplan-Meier Plotter databases were additionally used to evaluate the prognostic values of BGN in patients with solid cancer and co-expression gene analysis was conducted using the protein-protein interaction networks of BGN. The present study observed that the mRNA expression levels of BGN were increased in bladder, brain and central nervous system, breast, colorectal, esophageal, gastric, head and neck, lung, ovarian and 28 subtypes of cancer compared with normal tissues. The increased expression of BGN was identified to be associated with a poor outcome in ovarian and gastric cancer. Based on the co-expression network, BGN was identified as the key gene in a 43-gene network. The present findings of increased expression of BGN in solid tumors and its positive association with poor outcome on patient survival indicate that BGN may serve as a prognostic marker and as a target for novel therapeutics for multiple types of cancer.

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Section: Discussionmentioning

confidence: 99%

Biglycan as a potential diagnostic and prognostic biomarker in multiple human cancers

Zhao

Yin

Zhao³

et al. 2020

Oncol Lett

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“…S7 B , C ). COL6A3, which is positively regulated downstream of PI3K-AKT signaling in ECs (38), was induced at 8 h in WT MLECs but not in Salm4 −/− MLECs (Supplemental Fig. S7 B , C ).…”

Section: Resultsmentioning

confidence: 99%

SALM4 regulates angiogenic functions in endothelial cells through VEGFR2 phosphorylation at Tyr1175

et al. 2019

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Angiogenesis depends on VEGF-mediated signaling. However, the regulatory mechanisms and functions of individual VEGF receptor 2 (VEGFR2) phosphorylation sites remain unclear. Here, we report that synaptic adhesion-like molecule 4 (SALM4) regulates a specific VEGFR2 phosphorylation site. SALM4 silencing in HUVECs and Salm4 knockout (KO) in lung endothelial cells (ECs) of Salm4 −/− mice suppressed phosphorylation of VEGFR2 tyrosine (Y) 1175 (Y1173 in mice) and downstream signaling upon VEGF-A stimulation. However, VEGFR2 phosphorylation at Y951 (Y949 in mice) and Y1214 (Y1212 in mice) remained unchanged. Knockdown and KO of SALM4 inhibited VEGF-A–induced angiogenic functions of ECs. SALM4 depletion reduced endothelial leakage, sprouting, and migratory activities. Furthermore, in an ischemia and reperfusion (I/R) model, brain injury was attenuated in Salm4 −/− mice compared with wild-type (WT) mice. In brain lysates after I/R, VEGFR2 phosphorylation at Y949, Y1173, and Y1212 were induced in WT brains, but only Y1173 phosphorylation of VEGFR2 was reduced in Salm4 −/− brains. Taken together, our results demonstrate that SALM4 specifically regulates VEGFR2 phosphorylation at Y1175 (Y1173 in mice), thereby fine-tuning VEGF signaling in ECs.—Kim, D. Y., Park, J. A., Kim, Y., Noh, M., Park, S., Lie, E., Kim, E., Kim, Y.-M., Kwon, Y.-G. SALM4 regulates angiogenic functions in endothelial cells through VEGFR2 phosphorylation at Tyr1175.

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“…A numbers of previous reports demonstrated that phosphorylation protein form of p-AKT [18][19][20][21][22], p-mTOR [23][24][25][26], p-p38 [27][28][29][30] Fig 3(A, B)). These results indicate that MASTL silencing could inhibit gastric cancer cell invasion and migration in vitro.…”

Section: Discussionmentioning

confidence: 99%

Silencing MASTL Inhibits Cell Proliferation and Migration of Gastric Cancer MGC-803 Cells Via Suprressing AKT, mTOR, p38 Signal Pathways

Niu

et al. 2020

Preprint

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Background: Microtubule-associated serine/threonine kinase (MASTL) functions to regulate chromosome condensation and mitotic progression. Emerging reports showed that aberrant MASTL expression is commonly implicated in various human cancers and act as an oncogene. This study aimed to discover the potential significance of MASTL in gastric cancer, and to uncover relevant mechanisms. Methods: Lentivirus MASTL-shRNA was constructed and infected into MGC-803 cells to analysis its influences on cell proliferation by Green fluorescent protein (GFP)-based cellomics and colony formation assay, cell invasion and migration by transwell assay, apoptosis and cell cycle by flow cytometry detection, respectively. Nude mice and fluorescence imaging were used to characterize the regulation of tumor growth in vivo. Affymetrix mRNA microarray assay combined KEGG enrichment analysis were used to screen relevant molecules related to MASTL silencing. Finally，several aberrantly expressed genes were validated by quantitative reverse transcription PCR(RT-qPCR)and western blot detection. Results: Silencing MASTL significantly inhibited cell proliferation, migration and invasion, arrested cell cycle at G1 stage. Silencing MASTL reduced tumor growth in nude mice, and fluorescence imaging indicated that the total radiant efficiency of mice in the Lv-shMAST group was markedly reduced compared with in mice in the Lv-shCtrl group in vivo. Affymetrix mRNA microarray assay revealed that 124 genes upregulated, 167 genes downregulated. RT-qPCR and western blotting validation showed that cyclin dependent kinase 6(CDK6), bone morphogenetic protein 2(BMP2), snail family transcriptional repressor 2(SNAI2), phosphorylation-mechanistic target of rapamycin kinase (p-mTOR), phosphorylation-AKT serine/threonine kinase (p-AKT) and phosphorylation-p38 kinase (p-p38) are downregulated, and cyclin dependent kinase inhibitor 1A (CDKN1A) is upregulated. Conclusions: Silencing MASTL could significantly inhibit cell growth, migration ability, induce apoptosis, arrest cell cycle at G1 stage, and the mechanisms of which were mediated via inactivation of mTOR, AKT, p38 signal pathways.

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Retracted: Silencing of COL1A2, COL6A3, and THBS2 inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the PI3k‐Akt signaling pathway

Cited by 115 publications

References 39 publications

Biglycan as a potential diagnostic and prognostic biomarker in multiple human cancers

Biglycan as a potential diagnostic and prognostic biomarker in multiple human cancers

SALM4 regulates angiogenic functions in endothelial cells through VEGFR2 phosphorylation at Tyr1175

Silencing MASTL Inhibits Cell Proliferation and Migration of Gastric Cancer MGC-803 Cells Via Suprressing AKT, mTOR, p38 Signal Pathways

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