Human-like hyperplastic prostate with low ZIP1 induced solely by Zn deficiency in rats

Fong, Louise Y.Y.; Jing, Ruiyan; Smalley, Karl J.; Wang, Zixuan; Taccioli, Cristian; Fan, Sili; Chen, Zhidong; Alder, Hansjüerg; Huebner, Kay; Farber, John L.; Fiehn, Oliver; Croce, Carlo M.

doi:10.1073/pnas.1813956115

Cited by 24 publications

(27 citation statements)

References 54 publications

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“…Studies have shown that the level of zinc in normal human prostates is about 15 times higher than in other tissues [ 13 ]. Low expression of SLC39A1 decreases the level of Zn 2+ in prostate cancer tissue, thereby reducing the level of citrate, and ultimately resulting in the malignant progression of prostate cancer [ 14 , 15 ]. Therefore, SLC39A1 may play an important role in tumor progression.…”

Section: Introductionmentioning

confidence: 99%

SLC39A1 contribute to malignant progression and have clinical prognostic impact in gliomas

Wang

Zhang

et al. 2020

Cancer Cell Int

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Background Gliomas are one of the most common primary tumors of the central nervous system, and have an unfavorable prognosis. SLC39A1 is a zinc ion transport protein which inhibits the progression of prostate cancer. By studying the role and mechanism of SLC39A1 in the progression of gliomas, perhaps a new therapeutic target can be provided for their treatment. Method The TCGA, CCGA, GSE16011, GSE44971 and GSE11260 data sets were employed to evaluate the expression level of SLC39A1 in paracancerous and glioma tissues. In addition, Kaplan–Meier analysis, Cox analysis, and the ESTIMATE and CIBERSORT algorithms were used to analyze its prognostic value and immune infiltration correlation. A CCK-8 and flow cytometer were used to measure the effects of SLC39A1 on U87 cell proliferation or apoptosis; RT-qPCR and western blot were used to detect its effects on the expression of MMP2\MMP9. Results SLC39A1 has up-regulated expression in glioma tissues. High SLC39A1 expression predicted significantly worse survival. Univariate and multivariate analysis show that SLC39A1 independently indicated poor prognosis in patients with gliomas. The expression of SLC39A1 is significantly correlated with clinical pathological parameters such as Grade, IDH mutation status, and 1p19q codeletion status. In vitro experimental results show that SLC39A1 promotes proliferation of glioma cells, inhibits their apoptosis, and promotes expression of MMP2\MMP9. In addition, it may affect infiltration of immune cells into the glioma microenvironment. Conclusion SLC39A1 may serve as a new prognostic biomarker and potential target for treatment of gliomas.

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Section: Introductionmentioning

confidence: 99%

SLC39A1 contribute to malignant progression and have clinical prognostic impact in gliomas

Wang

Zhang

et al. 2020

Cancer Cell Int

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“…ChemRICH. Chemical set enrichment statistical analysis was performed on metabolomics data as described (42,49).…”

Section: Gene Expressionmentioning

confidence: 99%

“…Metabolome Network Visualization. Using KEGG and PubChem CIDs, a biochemical and chemical similarity network (37,49) was calculated for all measured metabolites.…”

Section: Gene Expressionmentioning

confidence: 99%

Abrogation of esophageal carcinoma development in miR-31 knockout rats

Fong

Taccioli

Palamarchuk

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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MicroRNA-31 (miR-31) is overexpressed in esophageal squamous cell carcinoma (ESCC), a deadly disease associated with dietary Zn deficiency and inflammation. In a Zn deficiency-promoted rat ESCC model with miR-31 up-regulation, cancer-associated inflammation, and a high ESCC burden followingN-nitrosomethylbenzylamine (NMBA) exposure, systemic antimiR-31 delivery reduced ESCC incidence from 85 to 45% (P= 0.038) and miR-31 gene knockout abrogated development of ESCC (P= 1 × 10−6). Transcriptomics, genome sequencing, and metabolomics analyses in these Zn-deficient rats revealed the molecular basis of ESCC abrogation by miR-31 knockout. Our identification of EGLN3, a known negative regulator of nuclear factor κB (NF-κB), as a direct target of miR-31 establishes a functional link between oncomiR-31, tumor suppressor target EGLN3, and up-regulated NF-κB–controlled inflammation signaling. Interaction among oncogenic miR-31, EGLN3 down-regulation, and inflammation was also documented in human ESCCs. miR-31 deletion resulted in suppression of miR-31–associated EGLN3/NF-κB–controlled inflammatory pathways. ESCC-free, Zn-deficient miR-31−/−rat esophagus displayed no genome instability and limited metabolic activity changes vs. the pronounced mutational burden and ESCC-associated metabolic changes of Zn-deficient wild-type rats. These results provide conclusive evidence that miR-31 expression is necessary for ESCC development.

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“…There were 1,276,106 new cases and 358,989 deaths (3.8% of all deaths caused by cancer in men) associated with PCa in 2018 (2). Risk factors for PCa include age, ethnicity, family history and diet; among those, age is the most consistent factor (3). The incidence of PCa is highest among older men, with millions of people suffering from this disease (4,5).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Lin

et al. 2020

Int J Oncol

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Prostate cancer (PCa) is the second leading cause of cancer-related death among men worldwide. The present study aimed to investigate the role of germ cell-specific gene 2 protein (GSG2), also termed histone H3 phosphorylated by GSG2 at threonine-3, in the development and progression of PCa. GSG2 expression levels in PCa tissues and para-carcinoma tissues was detected by immunohistochemistry. The GSG2 knockdown cell model was constructed by lentivirus infection, and the knockdown efficiency was verified by qPCR and WB. In addition, the effects of shGSG2 on cell proliferation, colony formation and apoptosis were evaluated by Celigo cell counting assay, Giemsa staining and flow cytometry, respectively. Tumor development in nude mice was also detected. GSG2 expression was upregulated in PCa tissues and human PCa cell lines PC-3 and DU 145. High expression of GSG2 in tumor samples was associated with progressed tumors. GSG2 knockdown suppressed cell proliferation and colony formation, but promoted apoptosis, which was also verified in vivo.The results of the present study revealed that GSG2 upregulation was associated with PCa progression; GSG2 knockdown inhibited cell proliferation and colony formation and induced apoptosis, and may therefore serve as a potential therapeutic target for PCa therapy.

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Human-like hyperplastic prostate with low ZIP1 induced solely by Zn deficiency in rats

Cited by 24 publications

References 54 publications

SLC39A1 contribute to malignant progression and have clinical prognostic impact in gliomas

SLC39A1 contribute to malignant progression and have clinical prognostic impact in gliomas

Abrogation of esophageal carcinoma development in miR-31 knockout rats

Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

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