ZNF280A promotes lung adenocarcinoma development by regulating the expression of EIF3C

Liu, Huan; Qin, Yingzhi; Zhou, Na; Ma, Dongjie; Wang, Yingyi

doi:10.1038/s41419-020-03309-9

Cited by 16 publications

(14 citation statements)

References 33 publications

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“…reported that ZNF280A was involved in the proliferation and tumorigenicity of CRC via inactivating the Hippo-signaling pathway, and Liu et al. found the promotion effect of ZNF280A in the development of lung adenocarcinoma by regulating the expression of EIF3C ( 4 , 12 ). Our findings revealed a novel mechanism that ZNF280A promoted the tumorigenesis of CRC by attenuating the ubiquitination and degradation of RPS14.…”

Section: Discussionmentioning

confidence: 99%

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Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14

et al. 2022

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Colorectal cancer (CRC), one of the cancers with highest mortality, involves complicated molecular mechanisms leading to the onset of malignant phenotypes. ZNF280A, a member of the zinc-finger protein family, was shown to be a promotor of oncogenesis in CRC in this study. ZNF280A was remarkably upregulated in CRC tissues, which was meaningfully associated with tumor progression and poor prognosis in patients with CRC. Loss-of-function studies revealed that ZNF280A knockdown inhibited the development and progression of CRC as evident by the inhibition of cell proliferation, colony formation, cell apoptosis, cell cycle distribution, and cell migration in vitro and the repressed tumorigenesis of CRC cells in vivo. Next, we showed that RPS14 was the downstream target of ZNF280A and ZNF280A knockdown promoted the ubiquitination as well as degradation of RPS14 in CRC. Additionally, we demonstrated that RPS14 regulated the development of CRC via PI3K-Akt signaling pathway. Taken together, our findings provide a novel clear insight into ZNF280A/RPS14/PI3K-Akt axis in CRC for the first time, offering a potential target for early detection, diagnosis and treatment of CRC in future clinical applications.

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Section: Discussionmentioning

confidence: 99%

“…ZNF280A is a member of the zinc-finger protein family, carrying a characteristic zinc-finger domain ( 4 ). Zinc finger proteins are the largest transcription factor family in human genome, playing a significant role in regulating and managing gene expression ( 5 , 6 ).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14

et al. 2022

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“…Some EIF3 subtypes have been suggested to influence cancer prognosis by affecting the proliferation and apoptosis of tumor cells [ 19 ]. ZNF280A may promote the development of lung adenocarcinoma by interacting with EIF3C, thus implying that EIF3C may have a potential role in lung cancer [ 12 ]. EIF3C is upregulated in renal cell carcinoma [ 20 ] and intrahepatic cholangiocarcinoma [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

EIF3C Promotes Lung Cancer Tumorigenesis by Regulating the APP/HSPA1A/LMNB1 Axis

et al. 2022

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Objective. This study was designed to explore the role and mechanism of eukaryotic initiation factor 3C (EIF3C) in the proliferation and apoptosis of lung cancer cells. Methods. EIF3C expression in clinic lung cancer tissues was detected by immunohistochemistry assay. Cell transfection with lentivirus EIF3C short hairpin RNA (shRNA) was performed with Lipofectamine 2000. Cell proliferation was evaluated by Celigo and MTT assays. Caspase-3/7 activity was assessed using caspase-3/7 assay kit for cell apoptosis detection. The apoptosis rate of lung cancer cells was assessed by flow cytometry. A transplanted tumor nude-mouse model was established to clarify the role of EIF3C in lung cancer. The potential mechanism of EIF3C was explored by mRNA microarray analysis. Among the top 30 up- and downregulated mRNAs selected for RT-qPCR, 5 were chosen for western blot analysis. Results. EIF3C was abnormally overexpressed in lung cancer cell lines and tissues. Silencing EIF3C suppressed the proliferation and promoted the apoptosis of lung cancer cells. In vivo experiments using transplanted tumor nude-mouse model suggested that EIF3C promoted lung cancer tumorigenesis. Further, mRNA microarray analyses identified 189 upregulated and 83 downregulated differentially expressed mRNA between the KD and negative control groups. After validation by RT-qPCR and western blot, three downstream genes (APP, HSPA1A, and LMNB1) were confirmed. Conclusion. EIF3C overexpression may facilitate the proliferation and hamper the apoptosis of lung cancer cells by regulating the APP/HSPA1A/LMNB1 axis.

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“…Moreover, patients with advanced lung adenocarcinoma are often accompanied by poor long-term prognosis. Currently, surgical resection plus radio-or chemotherapy represents the first choice and main therapeutic means against LUAD (5,6). Despite recent advances in immunotherapeutic strategies, LUAD patients display diverse responses to immune-based therapies (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Development of a Prognostic Alternative Splicing Signature Associated With Tumor Microenvironment Immune Profiles in Lung Adenocarcinoma

et al. 2022

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BackgroundAlternative splicing (AS), a pivotal post-transcriptional process across more than 95% of human transcripts, is involved in transcript structural variations and protein complexity. Clinical implications of AS events and their interaction with tumor immunity were systematically analyzed in lung adenocarcinoma (LUAD).MethodsTranscriptome profiling as well as AS data of LUAD were retrospectively curated. Then, the network of the overall survival (OS)-relevant AS events with splicing factors was established. After screening OS-relevant AS events, a LASSO prognostic model was conducted and evaluated with ROC curves. A nomogram that integrated independent prognostic indicators was created. Immune response and immune cell infiltration were estimated with ESTIMATE, CIBERSORT, and ssGSEA algorithms. Drug sensitivity was inferred with pRRophetic package.ResultsIn total, 2415 OS-relevant AS events were identified across LUAD patients. The interaction network of splicing factors with OS-relevant AS events uncovered the underlying regulatory mechanisms of AS events in LUAD. Thereafter, a prognostic model containing 12 AS events was developed, which acted as a reliable and independent prognostic indicator following verification. A nomogram that constituted stage and risk score displayed great effectiveness in evaluating the survival likelihood. Moreover, the AS-based prognostic model was in relation to immune response and immune cell infiltration. Patients with a high-risk score displayed therapeutic superiority to cisplatin, erlotinib, gefitinib, and gemcitabine. Finally, three AS-relevant genes (CDKN2A, TTC39C, and PKIB) were identified as prognostic markers.ConclusionCollectively, our findings developed an AS event signature with powerful prognostic predictive efficacy in LUAD.

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ZNF280A promotes lung adenocarcinoma development by regulating the expression of EIF3C

Cited by 16 publications

References 33 publications

Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14

Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14

EIF3C Promotes Lung Cancer Tumorigenesis by Regulating the APP/HSPA1A/LMNB1 Axis

Development of a Prognostic Alternative Splicing Signature Associated With Tumor Microenvironment Immune Profiles in Lung Adenocarcinoma

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