Proteomics-based identification of VDAC1 as a tumor promoter in cervical carcinoma

Zhang, Chang-lin; Ding, Wencheng; Liu, Yuan; Hu, Zheng; Zhu, Da; Wang, Xiaoli; Yu, Lan; Wang, Liming; Shen, Hui; Zhang, Weican; Ren, Chao; Li, Kezhen; Weng, Danhui; Deng, Wuguo; Ma, Ding; Wang, Hui

doi:10.18632/oncotarget.10562

Cited by 15 publications

(11 citation statements)

References 44 publications

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“…Cancer is a metabolic disease, and mitochondrial dysfunction is a common feature of cancer (27). A previous study reported that the expression of VDAC1 in tumor tissue, including liver cancer (8), non-small cell lung cancer (9) and cervical cancer (10), was higher compared with that in corresponding normal tissue, and that the protein controlled the fate of cancer cells (20). The results of the present study demonstrated that knockdown of VDAC1 inhibited the proliferation of breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

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VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer

Yang¹,

Zhou

et al. 2019

Oncol Lett

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Voltage-dependent anion channels (VDACs) are situated in the outer membrane of the mitochondria and serve as gatekeepers that control metabolite and ion exchange between the cytosol and mitochondria. VDAC1 is one of the most studied members of the VDAC protein family and is overexpressed in multiple types of cancer. However, the specific biological function and regulatory mechanism of VDAC1 in breast cancer remains unclear. The present study investigated the biological role of VDAC1 in breast cancer cells using an MTS assay. The association of clinicopathological features with VDAC1 in breast cancer was analyzed by Gene Expression Profiling Interactive Analysis. The regulatory mechanism of VDAC1 was determined by cell transfection, western blot analysis, reverse transcription-quantitative (q)PCR analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR analysis. The results of the present study demonstrated that VDAC1 promoted breast cancer proliferation and was associated with a poor prognosis in patients with breast cancer. Additionally, it was observed that the expression of VDAC1 could be decreased by the bromodomain inhibitor (JQ1), and bromodomain-containing protein 4 (BRD4) was indicated to be a regulator of VDAC1. Furthermore, results suggested that VDAC1 may be involved in the resistance of breast cancer to JQ1. Collectively, the present findings uncovered important aspects of the function of VDAC1 in the tumor progression of breast cancer, and may provide a basis for potential therapeutic strategies for the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%

“…non-small cell lung cancer (9). and cervical cancer (10). and that it promotes tumor growth and apoptosis (7,8).…”

Section: Introductionmentioning

confidence: 99%

VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer

Yang¹,

Zhou

et al. 2019

Oncol Lett

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“…Although it is known that cervical carcinoma and precancerous lesions are closely related with HPV infection, HPV-related proteomics is still in its infancy [ 29 ]. The detection rate of high-risk HPV subtypes (such as HPV 16 or 18) in Uygur women with cervical carcinoma is high (78 ~ 88 %), approaching the level of cervical carcinoma in high incidence areas [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Discovery and validation of FBLN1 and ANT3 as potential biomarkers for early detection of cervical cancer

Hao

Xiaona

et al. 2021

Cancer Cell Int

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Background To validate markers for cervical carcinoma (CC) and precancerous lesions related with HPV infections. Methods Three different cervical cancer cell lines C-33A, SiHa and Caski were used for secretome profiling by label-free quantitative proteomics. Cervical exfoliated cells and matching serum samples were collected from 284 patients with normal control (n = 75, 26.41 %), precancerous lesions (n = 88, 30.99 %) and early stage cervical squamous carcinoma (n = 121, 42.61 %). HPV subtyping and quantification was performed by PCR and hybridization. 20 candidate proteins identified in previous screening studies (tissue, plasma, cells) were quantified by ELISA. Finally, highly quantitative parallel reaction monitoring mass spectrometry was used to assess the specificities and sensitivities of candidate serum markers. Results While CC was found to be associated with high-risk HPV subtypes, serum antibodies for high risk HPV were not significantly related to the progression of cervical cancer. Significant differences between patient groups were detected for the four proteins CLU, APOA4, APOE and MLH3, but none would allow clinical application due to insufficient sensitivity and specificity and large variability. Subsequent proteomic secretome analysis of cervical cancer cell lines identified a set of 729 common proteins. Cross referencing this dataset with ELISA measurements revealed six candidate proteins of which two, FBLN1 and ANT3, showed co-occurrence with HPV infection (75.7 % and 85 %, respectively) and had promising diagnostic ability in terms of sensitivity and specificity. After the loss of E6/E7 by using CRISPR/Cas9 gene editing, the content of ANT3 and FBLN1 in KoE6/E7 SiHa were downregulated, which indicated the expression of ANT3 and FBLN1 in cervical cancer may be affected by HPV infection. Conclusions FBLN1 and ANT3 might be potential tumor- and HPV-associated serum markers.

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“…Because overexpression of VDAC1 triggers cell death, It may be related to the destruction of nerve cells 35 . VDAC1 was identi ed as a tumor promoter in cervical cancer, as well as knock-down of VDAC1 in cervical cancer Cell lines increase the rate at which apoptosis occurs, which was partially reversed by overexpression of VDAC1 36 .…”

Section: Discussionmentioning

confidence: 99%

Hsa-circ-0064636 regulation of the target gene VDAC1/UBE4A by hsa-miR-326/hsa-miR-503-5 in osteosarcoma

Yan

Huang

et al. 2021

Preprint

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Background: Circular RNAs (circRNAs) are a subclass of noncoding RNAs that play a critical role in the regulation of gene expression in eukaryotic organisms. Recent studies have revealed the critical role of circRNAs in cancer progression. Yet, little is not well understood of hsa-circ-0064636 in osteosarcoma (OS).Methods: The differential expression of hsa-circ-0064636 in OS cell lines was verified by quantitative real-time PCR (qRT-PCR). Differentially expressed mRNAs and miRNAs were screened in OS mRNA and miRNA expression datasets. miRNAs that interacted with hsa-circ-0064636 were predicted by RNAhybrid, TargetScan and miRanda. and were further detected using RNAhybrid, TargetScan and miRanda. miRWalk, miRMap, and miRNAMap were used to perform target gene prediction on the intersected miRNAs to construct a circ-miRNA-mRNA interactor network. The target genes were then subjected to survival analysis using PROGgeneV2, which resulted in a circ-miRNA-mRNA interaction subnetwork with prognostic impact.Results: The qRT-PCR experiments successfully verified that hsa-circ-0064636 was significantly overexpressed in the OS cell line. Hsa-mir-326(miR-326) and hsa-mir-503-5p(miR-503-5p) are target miRNAs of hsa-circ-0064636 in the target genes obtained from the miR-326 and miR-503-5p screens. UBE4A and VDAC1 had a significant effect on prognosis. UBE4A is a target gene for miR-326, while VDAC1 is a target gene for miR-503-5p .Conclusion: hsa-circ-0064636 may be involved in OS development through acting as a sponge to inhibit miR-326 and miR-503-5p , thus regulating the expression of VDAC1 and UBE4A.

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Proteomics-based identification of VDAC1 as a tumor promoter in cervical carcinoma

Cited by 15 publications

References 44 publications

VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer

VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer

Discovery and validation of FBLN1 and ANT3 as potential biomarkers for early detection of cervical cancer

Hsa-circ-0064636 regulation of the target gene VDAC1/UBE4A by hsa-miR-326/hsa-miR-503-5 in osteosarcoma

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