<i>Retracted:</i> <scp>GNA</scp>13 promotes tumor growth and angiogenesis by upregulating <scp>CXC</scp> chemokines via the <scp>NF</scp>‐κB signaling pathway in colorectal cancer cells

Zhang, Zhongqiang; Tan, Xiao; Luo, Jing; Cui, Beibei; Lei, Sanlin; Si, Zhongzhou; Shen, Liangfang; Yao, Hongliang

doi:10.1002/cam4.1783

Cited by 49 publications

(52 citation statements)

References 33 publications

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“…Western blotting was performed as previously described [33,34]. Brie y, cell lysis was performed with the RIPA buffer protein extraction reagent (Pierce, Rockford, IL, USA) containing a protease inhibitor cocktail (Roche, USA).…”

Section: Western Blottingmentioning

confidence: 99%

SETDB1 promotes glioblastoma growth via CSF-1 - dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Han

Wei

Guo

et al. 2020

Preprint

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Background: Glioblastoma is a common disease of the central nervous system (CNS), with high morbidity and mortality. In the infiltrate in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant, which are important factors in glioblastoma progression. However, the exact details of TAMs in glioblastoma progression have yet to be determined. Methods: The clinical relevance of SET domain bifurcated 1 (SETDB1) was analyzed by immunohistochemistry, real-time PCR and Western blotting of glioblastoma tissues. SETDB1-induced cell proliferation, migration and invasion were investigated by CCK-8 assay, colony formation assay, wound healing and Transwell assay. The relationship between SETDB1 and colony stimulating factor 1 (CSF-1), as well as TAMs recruitment was examined by Western blotting, real-time PCR and syngeneic mouse model.Results: Our findings showed that SETDB1 upregulated in glioblastoma and relative to poor progression. Gain and loss of function approaches showed the SETDB1 overexpression promotes cell proliferation, migration and invasion in glioblastoma cells. However, knockdown SETDB1 exerted opposite effects in vitro. Moreover, SETDB1 promotes AKT/mTOR-dependent CSF-1 induction and secretion, which leads to macrophage recruitment in the tumor, resulted in tumor growth. Conclusion: Our research clarified that SETDB1 regulates of tumor microenvironment and hence presents a potential therapeutic target for treating glioblastoma.

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Section: Western Blottingmentioning

confidence: 99%

SETDB1 promotes glioblastoma growth via CSF-1 - dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

Han

Wei

Guo

et al. 2020

Preprint

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“…Western blotting was performed as previously described [29,30]. Brie y, cell lysis was performed with the RIPA buffer protein extraction reagent (Pierce, Rockford, IL, USA) containing a protease inhibitor cocktail (Roche, USA).…”

Section: Western Blottingmentioning

confidence: 99%

SETDB1 Promotes the Growth of Glioma via CSF-1-dependent Macrophage Recruitment by Activating the AKT/mTOR Signaling Pathway

Han

Wei

Guo

et al. 2020

Preprint

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Background: Glioma is a common disease of the central nervous system (CNS), with high morbidity and mortality. Among the infiltrates in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant and they are significant factors in glioma progression. However, the exact details of disease progression have yet to be determined. Methods: The clinical relevance of SETDB1 was analyzed by immunohistochemistry, real-time PCR and Western blotting and of glioma cancer tissues. Tumor cell proliferation, migration and invasion were investigated by MTS assay, colony formation assay, xenograft, wound healing and Transwell assay. The relationship between SETDB1 and CSF-1, as well as TAMS was examined by Western blotting, real-time PCR and syngeneic mouse model.Results: This work shows the presence and upregulation of SETDB1 in gliomaand its relationship with disease prognosis. Gain and loss of function approaches showed the inhibition of apoptosis and the promotion of growth, migration and invasion of the disease with SETDB1 overexpression and converse effects with SETDB1 silencing in vitro. Mechanistically, SETDB1 promotes CSF-1 expression by activating the AKT/mTOR signaling pathway. This leads to macrophage recruitment in the tumor, leading to tumor growth. Conclusion: This studyclarifies the modulation of tumor functions by SETDB1 and hence presents a future avenue for treating glioma.

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“…MTT (3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was performed to analysis the cell viability according to the previously reported protocol (23,24). In brief, the cells were cultured in 96well plates.…”

Section: Cell Viability Assaymentioning

confidence: 99%

“…The in vivo study was carried out as mentioned previously (23). The treatments include alpelisib (20 mg/kg/day, oral gavage), perifosine (15 mg/kg/day, oral gavage), alone, vehicle control, or the combination of alpelisib and perifosine.…”

Section: Xenograft Modelmentioning

confidence: 99%

Alpelisib Inhibits PIK3CA-Mutant Breast Cancer Growth Through AKT-Dependent Bim Induction and Mcl-1 Degradation

Tan¹,

Zhang²,

Liu³

et al. 2020

Preprint

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Abstract Background: PIK3CA mutations are common genomic alterations in estrogen receptor (ER)-positive breast cancers, currently, the development of selective PI3Kα (phosphatidylinositol 3-kinase α) inhibitors is ongoing. The mechanisms contributing to the anticancer activity of alpelisib in PIK3CA-mutant breast cancer cells and the mechanism of acquired resistance to alpelisib remain elusive. Methods: Drug-sensitive cell lines were exposed to alpelisib to establish alpelisib-resistant cell lines. Western blotting was used to assess changes in protein expression. Apoptosis was evaluated by ﬂow cytometry. In vivo with mouse xenograft models and in vitro colony formation and MTS and assay were carried out to determine the growth inhibitory effects of the tested drugs. Protein half-lives were examined and proteasome inhibitors were used to estimate protein degradation. Gene knockdown was carried out using shRNA or siRNA. Results: In the present study, we report the potent induction of apoptosis by alpelisib in PIK3CA-mutant breast cancer cell lines. AKT phosphorylation suppression, AKT/Foxo3a-dependent Bim induction, and AKT/GSK-3β-dependent Mcl-1 degradation were observed. Apoptosis induced by alpelisib was attenuated by Mcl-1 (4A) overexpression or Bim suppression. Furthermore, alpelisib could not modulate Mcl-1 or Bim levels in cell lines that were resistant to alpelisib. AKT inhibitor and alpelisib combination restored the sensitivity of alpelisib-resistant cells to growth inhibition and apoptosis in vitro and in vivo. Conclusions: Therefore, modulation of Mcl-1 degradation and AKT-dependent Bim induction are crucial for mediating the resistance and sensitivity of PIK3CA-mutant breast tumor cells to alpelisib, thus making it a productive strategy for overcoming acquired resistance to alpelisib.

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Retracted: GNA13 promotes tumor growth and angiogenesis by upregulating CXC chemokines via the NF‐κB signaling pathway in colorectal cancer cells

Cited by 49 publications

References 33 publications

SETDB1 promotes glioblastoma growth via CSF-1 - dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

SETDB1 promotes glioblastoma growth via CSF-1 - dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

SETDB1 Promotes the Growth of Glioma via CSF-1-dependent Macrophage Recruitment by Activating the AKT/mTOR Signaling Pathway

Alpelisib Inhibits PIK3CA-Mutant Breast Cancer Growth Through AKT-Dependent Bim Induction and Mcl-1 Degradation

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