Knockdown of the Potential Cancer Stem-Like Cell Marker Rex-1 Improves Chemotherapeutic Effects in Gliomas

Kim, Bong-Sun; Kang, Kyung-Sun; Choi, Jin Hee; Jung, Jin-Sun; Im, Young-Bin; Kang, Soo‐Kyung

doi:10.1089/hum.2011.096

Cited by 11 publications

(7 citation statements)

References 38 publications

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“…The function of REX1 in cancer is still controversial. REX1 in prostate cancer, renal carcinoma and ESCC migh be a tumor suppressor gene, but in glioblastoma multiforme REX1 is an oncogene [16][17][18][19]32]. As we known, REX1 is a zinc finger protein of YY1 family.…”

Section: Discussionmentioning

confidence: 99%

“…On the one hand, REX1 can act as an antioncogene in prostate cancer, clear cell renal cell carcinoma, and esophageal squamous cell carcinoma (ESCC) [16][17][18]. On the other hand, REX1 can act as an oncogene in malignant glioblastoma multiforme patients by inducing p38/JNK and AKT/PI3K/GSK3β signaling and by leading to apoptosis [19]. As far as we known, there is no report on the function of REX1 in cervical carcinoma.…”

Section: Introductionmentioning

confidence: 99%

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REX1 promotes EMT-induced cell metastasis by activating the JAK2/STAT3-signaling pathway by targeting SOCS1 in cervical cancer

et al. 2019

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ZFP42 zinc finger protein (REX1), a pluripotency marker in mouse pluripotent stem cells, has been identified as a tumor suppressor in several human cancers. However, the function of REX1 in cervical cancer remains unknown. Both IHC and western blot assays demonstrated that the expression of REX1 protein in cervical cancer tissue was much higher than that in normal cervical tissue. A xenograft assay showed that REX1 overexpression in SiHa and HeLa cells facilitated distant metastasis but did not significantly affect tumor formation in vivo. In addition, in vitro cell migration and invasion capabilities were also promoted by REX1. Mechanistically, REX1 overexpression induced epithelial-to-mesenchymal transition (EMT) by upregulating VIMENTIN and downregulating E-CADHERIN. Furthermore, the JAK2/STAT3signaling pathway was activated in REX1-overexpressing cells, which also exhibited increased levels of p-STAT3 and p-JAK2, as well as downregulated expression of SOCS1, which is an inhibitor of the JAK2/STAT3-signaling pathway, at both the transcriptional and translational levels. A dual-luciferase reporter assay and qChIP assays confirmed that REX1 transsuppressed the expression of SOCS1 by binding to two specific regions of the SOCS1 promoter. Therefore, all our data suggest that REX1 overexpression could play a crucial role in the metastasis and invasion of cervical cancer by upregulating the activity of the JAK2/STAT3 pathway by trans-suppressing SOCS1 expression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

REX1 promotes EMT-induced cell metastasis by activating the JAK2/STAT3-signaling pathway by targeting SOCS1 in cervical cancer

et al. 2019

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“…REX1 is also called zinc finger protein 42 (ZFP42) (Jiang et al, 2002) and has been studied in multiple cancer types (Kim et al, 2011). Steve TLUK et al found that REX1 was frequently downregulated in HCC tumors.…”

Section: Rex1mentioning

confidence: 99%

Recent Advances in Liver Cancer Stem Cells: Non-coding RNAs, Oncogenes and Oncoproteins

Zhu

2020

Front. Cell Dev. Biol.

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Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide, with high morbidity, relapse, metastasis and mortality rates. Although liver surgical resection, transplantation, chemotherapy, radiotherapy and some molecular targeted therapeutics may prolong the survival of HCC patients to a certain degree, the curative effect is still poor, primarily because of tumor recurrence and the drug resistance of HCC cells. Liver cancer stem cells (LCSCs), also known as liver tumor-initiating cells, represent one small subset of cancer cells that are responsible for disease recurrence, drug resistance and death. Therefore, understanding the regulatory mechanism of LCSCs in HCC is of vital importance. Thus, new studies that present gene regulation strategies to control LCSC differentiation and replication are under development. In this review, we provide an update on the latest advances in experimental studies on non-coding RNAs (ncRNAs), oncogenes and oncoproteins. All the articles addressed the crosstalk between different ncRNAs, oncogenes and oncoproteins, as well as their upstream and downstream products targeting LCSCs. In this review, we summarize three pathways, the Wnt/β-catenin signaling pathway, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, and interleukin 6/Janus kinase 2/signal transducer and activator of transcription 3 (IL6/JAK2/STAT3) signaling pathway, and their targeting gene, c-Myc. Furthermore, we conclude that octamer 4 (OCT4) and Nanog are two important functional genes that play a pivotal role in LCSC regulation and HCC prognosis.

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“…Rex is a marker of pluripotency of embryonic cells. Its expression decreases with the degree of cell differentiation [4]. A number of stem cell markers, including cancer and specifically GBM, have been identified and well described in literature.…”

Section: Gfap Is An Intermediate Filament Protein Its Expressionmentioning

confidence: 99%

“…CD133, Nestin, βIII-tubulin, as well as markers of glial cells, for example GFAP. Currently, it is being suggested that transcription factors such as Nanog, Oct-4, Rex and Olig2 can be used as biomarkers of cancer stem cells and help identify these cells in a tumor mass [3][4][5]. CD133 is a transmembrane cell-surface glycoprotein.…”

Section: Introductionmentioning

confidence: 99%

Biomarkers of Cancer Stem Cells in Glioblastoma Multiforme and Histological Picture of Cancer

Wańkowicz¹,

Machaliński

Rogińska

et al. 2019

BJSTR

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Introduction: Glioblastoma (GBM) is the most aggressive primary brain cancer. A number of stem cell markers, including cancer and specifically GBM, have been identified and well described in literature. However, no attempts have been made to determine a relation between the expression of cancer stem cell markers in GBM and morphological features of this tumor. Therefore, the present study attempts to compare the expression of stem cell markers found in GBM tissue with selected features of tumor malignancy.Material and Methods: 21 GBM samples were tested. In the assessment of GBM histological features, the following were considered: nuclear pleomorphism, Ki-67 labeling index and endothelial proliferation. The expression of CD133, GFAP, Nestin, βIIItubulin, Oct-4, Nanog, Olig2 and Rex was analyzed by reverse transcription polymerase chain reaction.Results: A significantly higher expression of CD133 (p = 0,0007) and Nestin (p = 0,0216) were found in GBM with evident nuclear pleomorphism. We found also significantly higher expression of CD133, Nestin and Olig2 in patients with a Ki-67 labeling index over 15% (p = 0.0033, p = 0.0101, and p = 0.0066). Conclusion:The expression of biomarkers of stem cells in GBM is associated with a greater severity of anaplasia and tumor proliferative activity. So, it can be assumed that the aggressiveness of GBM is at least partly due to the presence of cancer stem cells in the tumor mass. Due to the resistance of these cells to radio-and chemotherapy, the described phenomena may be associated with lower therapeutic efficacy in patients with GBM.

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Knockdown of the Potential Cancer Stem-Like Cell Marker Rex-1 Improves Chemotherapeutic Effects in Gliomas

Cited by 11 publications

References 38 publications

REX1 promotes EMT-induced cell metastasis by activating the JAK2/STAT3-signaling pathway by targeting SOCS1 in cervical cancer

REX1 promotes EMT-induced cell metastasis by activating the JAK2/STAT3-signaling pathway by targeting SOCS1 in cervical cancer

Recent Advances in Liver Cancer Stem Cells: Non-coding RNAs, Oncogenes and Oncoproteins

Biomarkers of Cancer Stem Cells in Glioblastoma Multiforme and Histological Picture of Cancer

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