The unusual yin-yang fashion of RIZ1/RIZ2 contributes to the progression of esophageal squamous cell carcinoma

Cui, Yuantao; Ding, Min; Dong, Siming; Wang, Yuanguo; Zhang, Peng

doi:10.1515/biol-2016-0019

Cited by 4 publications

(4 citation statements)

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“…The imbalance expression of RIZ1/RIZ2 contributes to the progression of ESCC. 18,19 The occurrence and development of ESCC is a complex process involving multiple factors, multiple genes changing and multiple stages of carcinogenesis. Mig-6 located in this region has tumor-inhibiting activity in a variety of malignant human cancers.…”

Section: Discussionmentioning

confidence: 99%

“…The deactivation of RIZ1 was associated with highly methylation in DNA promoter region and could induce imbalance expression of RIZ1/RIZ2. The imbalance expression of RIZ1/RIZ2 contributes to the progression of ESCC 18,19 . The occurrence and development of ESCC is a complex process involving multiple factors, multiple genes changing and multiple stages of carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Mig‐6 could inhibit cell proliferation and induce apoptosis in esophageal squamous cell carcinoma

et al. 2021

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Background To investigate the expression and biological functions of mitogen‐induced gene 6 (Mig‐6) in esophageal squamous cell carcinoma (ESCC). Methods The expression of Mig‐6 in ESCC tissues and normal esophageal epithelial tissues were measured by immunohistochemistry (IHC) assay. MTT test was applied to detect the proliferative ability of ESCC cells after Mig‐6 was upregulated by transfection. A fluid cytology assay was used to detect apoptosis of ESCC cells. Agilent whole human genome oligo microarray was used to screen different expressed genes and the possible signaling pathways which might be involved. Results The expression of Mig‐6 protein was lower in ESCC tissues compared to normal esophageal epithelial tissues. Mig‐6 could restrain the ESCC cell growth and induce cell apoptosis. PPAR, CAMs and MAPK signaling pathways might be involved. Conclusions Mig‐6 might be a new tumor suppressor gene and a possible target for the specific therapy of ESCC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mig‐6 could inhibit cell proliferation and induce apoptosis in esophageal squamous cell carcinoma

et al. 2021

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“…Hence, further research to identify novel biomarkers should be performed. thyroid carcinoma (Cheng et al 2010;Cui et al 2016;Johansson et al 2018;Lal et al 2006;Michalak & Visvader 2016;Oshimo et al 2004;Pandzic et al 2017;Rossi et al 2009;Sakurada et al 2001;Tan et al 2014;Wu et al 2016;Yang et al 2017;Zhang et al 2016). Furthermore, in a meta-analysis that found a total of 22 genes methylated in hepatocellular carcinoma, PRDM2 was one of the genes with the most significant result and is on par with the well-known APC and p16 (Zhang et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Peer Review #2 of "The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis (v0.1)"

2020

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Background. Many studies have reported the presence of Positive Regulatory/Su(var)3-9,Enhancer-of-zeste and Trithorax Domain 2 (PRDM2) downregulation in cancer. However, its potential as a diagnostic biomarker is still unclear. Hence, a systematic review and metaanalysis were conducted to address this issue. Introduction. As of 2018, cancer has become the second leading cause of death worldwide. Thus, cancer control is exceptionally vital in reducing mortality. One such example is through early diagnosis of cancer using tumor biomarkers. Having a function as a tumor suppressor gene (TSG), PRDM2 has been linked with carcinogenesis in several solid tumor. This study aims to assess the relationship between PRDM2 downregulation and solid tumor, its relationship with clinicopathological data, and its potential as a diagnostic biomarker. This study also aims to evaluate the quality of the studies, data reliability and confidence in cumulative evidence. Materials & Methods. A protocol of this study is registered at the International Prospective Register of Systematic Reviews (PROSPERO) with the following registration number: CRD42019132156. PRISMA was used as a guideline to conduct this review. A comprehensive electronic search was performed from inception to June 2019 in Pubmed, Cochrane Library, ProQuest, EBSCO and ScienceDirect. Studies were screened and included studies were identified based on the criteria made. Finally, data synthesis and quality assessment were conducted. Results. There is a significant relationship between PRDM2 downregulation with solid tumor (RR 4.29, 95% CI 2.58-7.13, P < 0.00001). The overall sensitivity and specificity of PRDM2 downregulation in solid tumors is 84% (95% CI 39-98%) and 86% (95% CI 71-94%), respectively. There is a low risk of bias for the studies used. TSA results suggested the presence of marked imprecision. The overall quality of evidence for this study is very low. Discussion. We present the first meta-analysis that investigated the potential of PRDM2 downregulation as a diagnostic biomarker in solid tumor. In line with previous studies, our results demonstrated that PRDM2 downregulation occurs in solid tumor. A major source of limitation in this study is the small number of studies. Conclusions. Our review suggested that PRDM2 is downregulated in solid tumor. The relationship between PRDM2 downregulation and clinicopathological data is still inconclusive. Although the sensitivity

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“…Its gene products are also involved in DNA-binding and transcription factor binding-activities, implicating its role in carcinogenesis (Sorrentino et al, 2018;Zhang et al, 2015). Studies have also reported PRDM2 downregulation in cancers that exhibit high incidence and mortality, such as bladder cancer, breast cancer, cervical cancer, colorectal cancer, endometrial cancer, esophageal squamous cell carcinoma, gastric carcinoma, hepatocellular carcinoma, lung cancer, pancreatic cancer, prostate cancer, T-cell prolymphocytic leukemia and thyroid carcinoma (Cheng, Gao & Lou, 2010;Cui et al, 2016;Johansson et al, 2018;Lal et al, 2006;Michalak & Visvader, 2016;Oshimo et al, 2004;Pandzic et al, 2017;Rossi et al, 2009;Sakurada et al, 2001;Tan et al, 2014;Wu et al, 2016;Yang et al, 2017;Zhang et al, 2016). Furthermore, in a meta-analysis that found a total of 22 genes methylated in hepatocellular carcinoma, PRDM2 was one of the genes with the most significant result and is on par with the well-known APC and p16 (Zhang et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis

Tanadi

Bambang

Wendi

et al. 2020

PeerJ

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Background Many studies have reported the presence of Positive Regulatory/Su(var)3-9, Enhancer-of-zeste and Trithorax Domain 2 (PRDM2) downregulation in cancer. However, its potential as a diagnostic biomarker is still unclear. Hence, a systematic review and meta-analysis were conducted to address this issue. Introduction As of 2018, cancer has become the second leading cause of death worldwide. Thus, cancer control is exceptionally vital in reducing mortality. One such example is through early diagnosis of cancer using tumor biomarkers. Having a function as a tumor suppressor gene (TSG), PRDM2 has been linked with carcinogenesis in several solid tumor. This study aims to assess the relationship between PRDM2 downregulation and solid tumor, its relationship with clinicopathological data, and its potential as a diagnostic biomarker. This study also aims to evaluate the quality of the studies, data reliability and confidence in cumulative evidence. Materials & Methods A protocol of this study is registered at the International Prospective Register of Systematic Reviews (PROSPERO) with the following registration number: CRD42019132156. PRISMA was used as a guideline to conduct this review. A comprehensive electronic search was performed from inception to June 2019 in Pubmed, Cochrane Library, ProQuest, EBSCO and ScienceDirect. Studies were screened and included studies were identified based on the criteria made. Finally, data synthesis and quality assessment were conducted. Results There is a significant relationship between PRDM2 downregulation with solid tumor (RR 4.29, 95% CI [2.58–7.13], P < 0.00001). The overall sensitivity and specificity of PRDM2 downregulation in solid tumors is 84% (95% CI [39–98%]) and 86% (95% CI [71–94%]), respectively. There is a low risk of bias for the studies used. TSA results suggested the presence of marked imprecision. The overall quality of evidence for this study is very low. Discussion We present the first meta-analysis that investigated the potential of PRDM2 downregulation as a diagnostic biomarker in solid tumor. In line with previous studies, our results demonstrated that PRDM2 downregulation occurs in solid tumor. A major source of limitation in this study is the small number of studies. Conclusions Our review suggested that PRDM2 is downregulated in solid tumor. The relationship between PRDM2 downregulation and clinicopathological data is still inconclusive. Although the sensitivity and specificity of PRDM2 downregulation are imprecise, its high values, in addition to the evidence that suggested PRDM2 downregulation in solid tumor, hinted that it might still have a potential to be used as a diagnostic biomarker. In order to further strengthen these findings, more research regarding PRDM2 in solid tumors are encouraged.

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The unusual yin-yang fashion of RIZ1/RIZ2 contributes to the progression of esophageal squamous cell carcinoma

Cited by 4 publications

References 18 publications

Mig‐6 could inhibit cell proliferation and induce apoptosis in esophageal squamous cell carcinoma

Mig‐6 could inhibit cell proliferation and induce apoptosis in esophageal squamous cell carcinoma

Peer Review #2 of "The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis (v0.1)"

The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis

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