Development of a multiplex MethyLight assay for the detection of DAPK1 and SOX1 methylation in epithelial ovarian cancer in a north Indian population

Kaur, Manpreet; Singh, Alka; Singh, Kiran; Gupta, Sameer; Sachan, Manisha

doi:10.1266/ggs.15-00051

Cited by 10 publications

(4 citation statements)

References 21 publications

(19 reference statements)

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“…Studies have also shown an inhibitory effect of SOX1 on a variety of tumors. In addition, many studies have shown that SOX1 can be used as a biomarker for a variety of tumors, such as cervical cancer, colon cancer, glioma, liver cancer, ovarian cancer, and small cell lung cancer [ 28 – 33 ]. However, to the best of our knowledge, the association between SOX1 and CCA has not been reported.…”

Section: Discussionmentioning

confidence: 99%

MiR-155-5p suppresses SOX1 to promote proliferation of cholangiocarcinoma via RAF/MEK/ERK pathway

Xiong

et al. 2021

Cancer Cell Int

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Background Accumulating evidence has demonstrated the close relation of SOX1 with tumorigenesis and tumor progression. Upregulation of SOX1 was recently shown to suppress growth of human cancers. However, the expression and role of SOX1 in cholangiocarcinoma (CCA) is not well characterized. Methods Expression levels of SOX1 in CCA tissues and normal bile duct tissues were examined using public GEO database. Western blot and immunohistochemistry were used to confirm the expression levels. Cell proliferation assay (CCK-8) and colony formation assay were performed to assess proliferation of CCA cells. A mouse model of subcutaneous transplantable tumors was used to evaluated proliferation of CCA in vivo. The putative regulating factor of SOX1 were determined using Targetscan and dual-luciferase reporter assay. Results SOX1 was downregulated in CCA tissues. Overexpression of SOX1 significantly inhibited cell proliferation in vitro and suppressed tumor growth in vivo. miR-155-5p directly targeted the 3′-untranslated region (3′UTR) of SOX1 and inhibited expression of SOX1, resulting in the activation of RAF, MEK and ERK phosphorylation, and thus CCA proliferation. However, restoration of SOX1 expression in miR-155-5p overexpressing cell lines decreased the phosphorylation level of RAF, MEK and ERK, as well as the proliferation of CCA cells. Conclusion MiR-155-5p decreased the expression of SOX1 by binding to its 3′UTR, which activated the RAF/MEK/ERK signaling pathway and promoted CCA progression.

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Section: Discussionmentioning

confidence: 99%

MiR-155-5p suppresses SOX1 to promote proliferation of cholangiocarcinoma via RAF/MEK/ERK pathway

Xiong

et al. 2021

Cancer Cell Int

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“…SOX1 is a member of the transcription factor sox family, which plays an important role in embryo and postnatal development. According to the current research, SOX1 also has a certain inhibitory effect on a variety of tumors, and many studies have proved that SOX1 can be used as a biomarker for a variety of tumors, such as cervical cancer, colon cancer, glioma, liver cancer, ovarian cancer, small cell lung cancer (24)(25)(26)(27)(28)(29), etc. But association between SOX1 and CCA has not been reported.…”

Section: Discussionmentioning

confidence: 99%

MiR-155-5p Suppress SOX1 to Promote the Proliferation of Cholangiocarcinoma via RAF/MEK/ERK Pathway

Wang¹,

Xiong²,

Wu³

et al. 2021

Preprint

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BackgroundAccumulating evidences indicate that SOX1 is closely related to tumorigenesis and development, upregulation of SOX1 is recently reported to suppress growth of human cancers. However, the expression and role of SOX1 in cholangiocarcinoma (CCA) remain unknown.MethodsThe expression levels of SOX1 in CCA tissues and normal bile duct tissues were examined by public GEO database, and western blot and immunohistochemistry were used to confirm the expression again. Cell proliferation assay (CCK-8) and colony formation assay were performed to determine proliferation of CCA cells. A model of transplatable subcutaneously tumors in mouse was used to evaluated proliferation of CCA in vivo. The putative regulating factor of SOX1 were disclosed by Targetscan and a dual-luciferase reporter assay.ResultsSOX1 was downregulated in CCA tissues. Overexpression of SOX1 significantly inhibited cell proliferation in vitro and tumor growth in vivo. Furthermore, miR-155-5p directly targets 3’UTR of SOX1 and inhibits expression of SOX1, resulting in the activation of RAF, MEK and ERK phosphorylation and thus CCA proliferation. However, when SOX1 expression was restored in miR-155-5p overexpressing cell lines, the phosphorylation level of RAF, MEK and ERK were decreased, as well as the proliferation of CCA cells.ConclusionMiR-155-5p could bind to the 3’UTR of SOX1 to decrease the expression of SOX1, and further activated the RAF/MEK/ERK signaling pathway to promote CCA progression.

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“…Previous researches have reported several biological mechanisms contribute to DAPK1's pro‐apoptotic character, especially in cases of cancer . For instance, DAPK1 affected the performance of the TNF‐α or IFN‐γ cascade in the ovarian cancer . Moreover, it has been demonstrated that inhibition of DAPK1 stimulates the apoptotic cell death and protects against ischemic neuronal damage that exhibited the potential effect of DAPK1 in ischemic injury .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐98 attenuates cardiac ischemia‐reperfusion injury through inhibiting DAPK1 expression

et al. 2018

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Cardiovascular ischemic disease is a large class of diseases that are harmful to human health. The significant role of microRNAs (miRNAs) in terms of controlling cardiac injury has been reported in latest studies. MiR‐98 is very important in regulating the apoptosis, the differentiation, the growth as well as the metastasis of cells. Nevertheless, the effect of miR‐98 in the cardiac ischemia reperfusion (I/R) injury has rarely been investigated. In the current research, we found that the miR‐98 expression was down‐regulated in the cardiomyocytes subjected to hypoxia/reoxygenation (H/R) and in the myocardium of the I/R rats. In addition, over‐expression of miR‐98 could significantly reduce the myocardial oxidative stress and ischemic injury as well as cell apoptosis. In agreement, similar findings were demonstrated in H9c2 cells subjected to H/R injury. Bioinformatic analysis using MiRanda and TargetScan and luciferase activity assay confirmed death‐associated protein kinase 1 (DAPK1) as a direct target of miR‐98. These findings suggest that miR‐98 may be exploited as a novel molecular marker or therapeutic target for myocardial I/R injury. © 2018 IUBMB Life, 71(1):166–176, 2019

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Development of a multiplex MethyLight assay for the detection of DAPK1 and SOX1 methylation in epithelial ovarian cancer in a north Indian population

Cited by 10 publications

References 21 publications

MiR-155-5p suppresses SOX1 to promote proliferation of cholangiocarcinoma via RAF/MEK/ERK pathway

MiR-155-5p suppresses SOX1 to promote proliferation of cholangiocarcinoma via RAF/MEK/ERK pathway

MiR-155-5p Suppress SOX1 to Promote the Proliferation of Cholangiocarcinoma via RAF/MEK/ERK Pathway

MicroRNA‐98 attenuates cardiac ischemia‐reperfusion injury through inhibiting DAPK1 expression

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