SOX7 Target Genes and Their Contribution to Its Tumor Suppressive Function

Zhang, Yumeng; Stovall, Daniel B.; Wan, Meimei; Zhang, Qiang; Chou, Jeff W.; Li, Dangdang; Sui, Guangchao

doi:10.3390/ijms19051451

Cited by 20 publications

(18 citation statements)

References 50 publications

(76 reference statements)

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“…In addition to activating p53, lncRNA MEG3 can improve the apoptosis of the tumor cells by reducing Bcl-xL (Liu et al, 2015). Besides, the transcription factor SOX7 acts as tumor suppressor in NSCLC possibly through activating SPRY1 and SLIT2, and repressing TRIB3 and MTHFD2 (Hayano et al, 2013;Zhang et al, 2018). MEG3 can enhance the sensitivity to DDP of NSCLC via MEG3/miR-21-5p/SOX7 axis (Wang et al, 2017a).…”

Section: Downregulated Lncrnas In Nsclc Ddp Resistancementioning

confidence: 99%

Long Non-Coding RNA in Drug Resistance of Non-Small Cell Lung Cancer: A Mini Review

et al. 2019

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Lung cancer is one of main causes of cancer mortality and 83% of lung cancer cases are classified as non-small cell lung cancer (NSCLC). Patients with NSCLC usually have a poor prognosis and one of the leading causes is drug resistance. With the progress of drug therapy, the emergence and development of drug resistance affected the prognosis of patients severely. Accumulating evidence reveals that long non-coding RNAs (lncRNAs), as "dark matters" of the human genome, is of great significance to drug resistance in NSCLC. Herein, we review the role of lncRNAs in drug resistance in NSCLC.

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Section: Downregulated Lncrnas In Nsclc Ddp Resistancementioning

confidence: 99%

Long Non-Coding RNA in Drug Resistance of Non-Small Cell Lung Cancer: A Mini Review

et al. 2019

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“…11 To determine whether Sox7 physically interacts with PSME in vivo, we carried out ChIP analysis in C4-2 cells with ectopic Sox7 expression using a ChIP-validated anti-Sox7 antibody. 25 Our data indicated that anti-Sox7 antibody preferentially precipitated the genomic region containing PSME compared to IgG control antibody ( Figure 3A). Furthermore, this difference was not observed when we used the same antibody pairs against a genomic region on chromosome 8 (SNP28254).…”

Section: Sox7 Interacts With Psme In Vivo and Negatively Regulates mentioning

confidence: 71%

“…PSMA expression is stimulated by an enhancer element, PSME , in prostate cells, which contains several potential binding sites for Sox proteins . To determine whether Sox7 physically interacts with PSME in vivo, we carried out ChIP analysis in C4‐2 cells with ectopic Sox7 expression using a ChIP‐validated anti‐Sox7 antibody . Our data indicated that anti‐Sox7 antibody preferentially precipitated the genomic region containing PSME compared to IgG control antibody (Figure A).…”

Section: Resultsmentioning

confidence: 94%

Sox7 negatively regulates prostate‐specific membrane antigen (PSMA) expression through PSMA‐enhancer

et al. 2018

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Background PSMA expression in the prostate epithelium is controlled by a cis‐element, PSMA enhancer (PSME). PSME contains multiple binding sites for Sox proteins, and in this study, we identified Sox7 protein as a negative regulator of PSMA expression through its interaction with PSME. Methods The statistical correlation between Sox7 and PSMA mRNA expression was evaluated using five prostate cancer studies from cBioportal. In vitro and in vivo interaction between Sox7 and PSME was evaluated by chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA), and luciferase reporter assay. Synthetic oligonucleotides were generated to define the sites in PSME that interact with Sox7 protein. Sox7 mutants were generated to identify the region of this protein required to regulate PSMA expression. Sox7 was also stably expressed in LNCaP/C4‐2 and 22Rv1 cells to validate the regulation of PSMA expression by Sox7 in vivo. Results Sox7 mRNA expression negatively correlated with PSMA/FOLH1 and PSMAL/FOLH1B mRNA expression in Broad/Cornell, TCGA and MSKCC studies, but not in two studies containing only metastatic prostate tumors. PC‐3 cells mostly expressed the 48.5 KDa isoform 2 of Sox7, and the depletion of this isoform did not restore PSMA expression. Ectopic expression of canonical, wild‐type Sox7 in C4‐2 and 22Rv1 cells suppressed PSMA protein expression. ChIP assay revealed that canonical Sox7 protein preferentially interacts with PSME in vivo, and EMSA identified the SOX box sites #2 and #4 in PSME as required for its interaction. Sox7 was capable of directly binding to PSME and suppressed PSME‐mediated transcription. The NLS regions of Sox7, but not its β‐catenin interacting motif, are essential for this suppressing activity. Furthermore, restoration of wild‐type Sox7 expression but not Sox7‐NLS mutant in Sox7‐null prostate cancer cell lines suppressed PSMA expression. Conclusions The inactivation of canonical Sox7 is responsible for the upregulated expression of PSMA in non‐metastatic prostate cancer.

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“…One is Sox7 that activates its targeted genes, such as SPRY1 and SLIT2 by serving as a transcriptional factor. 46 The other is Sox7 antagonism of Wnt/β-catenin signaling, a commonly upregulated pathway in human cancers involved in the regulation of cell proliferation, survival, and migration. 45 , 47 , 48 But the precise molecular mechanism behind these effects remains unclear.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-494-3p Promotes Cell Growth, Migration, and Invasion of Nasopharyngeal Carcinoma by Targeting Sox7

Liao

Yang

et al. 2018

Technol Cancer Res Treat

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Background:There is mounting evidence that microRNAs play an important role in nasopharyngeal carcinoma, which is widely prevalent in South China and is the most prevalent metastatic cancer among head and neck cancers. Recently, it has been shown that miR-494 is involved in the progression and prognosis of nasopharyngeal carcinoma. However, little is known about the function and mechanism of miR-494-3p in nasopharyngeal carcinoma. In the present study, we aimed to investigate the effects of miR-494-3p on the migration and invasion of nasopharyngeal carcinoma and to further explore the underlying mechanisms of these processes.Methods:The expression levels of miR-494-3p and Sox7 in nasopharyngeal carcinoma specimens and nasopharyngeal carcinoma cell lines were measured using quantitative reverse transcription polymerase chain reaction. Luciferase reporter assay, quantitative reverse transcription polymerase chain reaction, and Western blotting were used to confirm whether Sox7 was a direct target of miR-494-3p. Additionally, the roles of miR-494-3p and Sox7 on cell proliferation, migration, and invasion of nasopharyngeal carcinoma were analyzed by Cell Counting Kit-8 (CCK-8) assay, wound healing assay, and Boyden chamber assay, respectively.Results:Our study demonstrated that miR-494-3p was commonly upregulated in nasopharyngeal carcinoma specimens and nasopharyngeal carcinoma cell lines compared with nontumor nasopharyngeal epithelial tissue or nasopharyngeal cells (NP69). Moreover, miR-494-3p negatively regulated Sox7 at the posttranscriptional level by binding to a specific site in the Sox7 3′-untranslated region. In addition, synthetic miR-494-3p mimics significantly promoted proliferation, migration, and invasion of S18 and S26 nasopharyngeal carcinoma cells, while a synthetic miR-494-3p inhibitor resulted in suppressed nasopharyngeal carcinoma cell migration and invasion.Conclusion:miR-494-3p promotes nasopharyngeal carcinoma cell growth, migration, and invasion by directly targeting Sox7. Our results suggest that miR-494-3p might be a potential therapeutic target for nasopharyngeal carcinoma.

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SOX7 Target Genes and Their Contribution to Its Tumor Suppressive Function

Cited by 20 publications

References 50 publications

Long Non-Coding RNA in Drug Resistance of Non-Small Cell Lung Cancer: A Mini Review

Long Non-Coding RNA in Drug Resistance of Non-Small Cell Lung Cancer: A Mini Review

Sox7 negatively regulates prostate‐specific membrane antigen (PSMA) expression through PSMA‐enhancer

MicroRNA-494-3p Promotes Cell Growth, Migration, and Invasion of Nasopharyngeal Carcinoma by Targeting Sox7

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