Oncogenic zinc finger protein <scp>ZNF687</scp> accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the <scp>PI3K</scp>/<scp>AKT</scp> signaling pathway

Li, Mingchun; Liu, Zhihua; Hou, Zan; Wang, Xiangcai; Shi, Huaqiu; Li, Yamei; Xiao, Xuewen; Tang, Zhixian; Yang, Jiajun; Luo, Yaoling; Zhang, Min-Hong; Chen, Ming

doi:10.1111/1759-7714.14856

Cited by 4 publications

(2 citation statements)

References 41 publications

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“…ZNF687 has been confirmed to be a facilitator in the progression of some cancers, [13][14][15][16] but its regulatory functions in CRC maintain dimness. This study found that ZNF687 had a higher expression in CRC tissues and cells, which contributed to the poor prognosis of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…13 Furthermore, ZNF687 activates the PI3K/AKT pathway to aggravate tumorigenesis in lung adenocarcinoma. 14 In addition, studies have indicated that ZNF687 exhibits higher expression and mutates in bone cancer and acute myeloid leukemia through its oncogenic function. 15,16 Nevertheless, no research has been investigated on the regulatory functions of ZNF687 in CRC progression.…”

Section: Introductionmentioning

confidence: 99%

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FTO‐mediated ZNF687 accelerates tumor growth, metastasis, and angiogenesis in colorectal cancer through the Wnt/β‐catenin pathway

Li,

Xing

et al. 2023

Biotech and App Biochem

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Colorectal cancer (CRC) is a common and lethal cancer. ZNF687 has been disclosed to take part in diversified cancers’ progression by serving as a facilitator. However, the detailed regulatory functions of ZNF687 in the CRC have not been investigated. This work is planned to probe the impacts of ZNF687 on CRC progression. The IHC, RT‐qPCR, and western blot assays were used to examine mRNA and protein gene expressions. The cell proliferation measurement was accompanied by a CCK‐8 assay. The Transwell assay was performed to evaluate cell invasion and migration. The angiogenesis ability was evaluated by a tube formation experiment. The m6A level was evaluated through MeRIP and m6A dot blot assays. The binding ability between ZNF687 and FTO (fat mass and obesity associated protein) was tested through an RIP assay. The β‐catenin nuclear translocation was assessed through an immunofluorescence assay. The tumor growth was evaluated through an in vivo assay. ZNF687 exhibited higher expression in CRC cells and resulted in a poor prognosis. Additionally, ZNF687 inhibition suppressed CRC cell proliferation, invasion, migration, and angiogenesis. Furthermore, the suppression of ZNF687 retarded the Wnt pathway. Through rescue assays, the reduced cell migration, proliferation, invasion, and angiogenesis mediated by ZNF687 knockdown could be reversed after BML‐284 (the activator of the Wnt pathway) treatment. Finally, it was explained that ZNF687 knockdown inhibited in vivo tumor growth. This study manifested that FTO‐mediated ZNF687 aggravated tumor growth, metastasis, and angiogenesis of CRC through Wnt/β‐catenin pathway. This finding may provide a hopeful molecular target for CRC treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

FTO‐mediated ZNF687 accelerates tumor growth, metastasis, and angiogenesis in colorectal cancer through the Wnt/β‐catenin pathway

Li,

Xing

et al. 2023

Biotech and App Biochem

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Systematic characterization of therapeutic vulnerabilities in Multiple Myeloma with Amp1q reveals increased sensitivity to the combination of MCL1 and PI3K inhibitors

Sklavenitis-Pistofidis

Lightbody

Reidy

et al. 2023

Preprint

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SUMMARYThe development of targeted therapy for patients with Multiple Myeloma (MM) is hampered by the low frequency of actionable genetic abnormalities. Gain or amplification of chr1q (Amp1q) is the most frequent arm-level copy number gain in patients with MM, and it is associated with higher risk of progression and death despite recent advances in therapeutics. Thus, developing targeted therapy for patients with MM and Amp1q stands to benefit a large portion of patients in need of more effective management. Here, we employed large-scale dependency screens and drug screens to systematically characterize the therapeutic vulnerabilities of MM with Amp1q and showed increased sensitivity to the combination of MCL1 and PI3K inhibitors. Using single-cell RNA sequencing, we compared subclones with and without Amp1q within the same patient tumors and showed that Amp1q is associated with higher levels ofMCL1and the PI3K pathway. Furthermore, by isolating isogenic clones with different copy number for part of the chr1q arm, we showed increased sensitivity to MCL1 and PI3K inhibitors with arm-level gain. Lastly, we demonstrated synergy between MCL1 and PI3K inhibitors and dissected their mechanism of action in MM with Amp1q.

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Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway

Liu

Hou

et al. 2023

Thoracic Cancer

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Background Zinc finger protein 687 (ZNF687) has previously been discovered as a potential oncogene in individuals with giant cell tumors of the bone, acute myeloid leukemia, and hepatocellular carcinoma. However, its role and mechanism in lung adenocarcinoma (LUAD) remain unclear. Methods In LUAD cells, tumor, and matched adjacent tissue specimens, quantitative real‐time RT‐ polymerase chain reaction (qRT‐PCR), western blotting analyses, and immunohistochemistry staining (IHC) were conducted. Cell counting kit‐8 (CCK8) assay, clonogenicity analysis, flow cytometry, and transwell assays were utilized to detect ZNF687 overexpression and knockdown impacts on cell growth, colony formation, cell cycle, migration, and invasion. Bioinformatic studies, qRT‐PCR and western blotting studies were employed to validate the underlying mechanisms and signaling pathways implicated in the oncogenic effect of ZNF687. Results This study demonstrated that ZNF687 expression was elevated in LUAD cells and tissues. Individuals with upregulated ZNF687 had a poorer prognosis than those with downregulatedZNF687 ( p < 0.001). ZNF687 overexpression enhanced LUAD growth, migration, invasion and colony formation, and the cell cycle G1‐S transition; additionally, it promoted the epithelial‐mesenchymal transition (EMT). In contrast, knocking down ZNF687 showed to have the opposite impact. Moreover, these effects were associated with the activity of the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) signaling mechanism. Conclusion ZNF687 was upregulated in LUAD, and high ZNF687 expression levels are associated with poor prognoses. The activation of the PI3K/AKT signaling pathway by upregulated ZNF687 increased the proliferation of LUAD cells and tumor progression. ZNF687 may be a beneficial predictive marker and a therapeutic target in LUAD.

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Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway

Cited by 4 publications

References 41 publications

FTO‐mediated ZNF687 accelerates tumor growth, metastasis, and angiogenesis in colorectal cancer through the Wnt/β‐catenin pathway

FTO‐mediated ZNF687 accelerates tumor growth, metastasis, and angiogenesis in colorectal cancer through the Wnt/β‐catenin pathway

Systematic characterization of therapeutic vulnerabilities in Multiple Myeloma with Amp1q reveals increased sensitivity to the combination of MCL1 and PI3K inhibitors

Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway

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