PTTG1: a Unique Regulator of Stem/Cancer Stem Cells in the Ovary and Ovarian Cancer

Parte, Seema; Virant‐Klun, Irma; Patankar, Manish S.; Batra, Surinder K.; Straughn, Alex R.; Kakar, Sham S.

doi:10.1007/s12015-019-09911-5

Cited by 19 publications

(14 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The biomarkers (CD133 + , CD15 + , WNT5, ABTG2 and MYCBP) of CSCs were identi ed in chordomas, [51], but these makers were not detected here. Instead, the biomarkers of CSCs such as STMN1, UB2C and PTTG1 in hepatocellular carcinoma, breast cancer, prostate tumors were detected here [31][32][33][34][35]. The pathological mechanisms of these markers should be further investigated in the future studies.…”

Section: Discussionmentioning

confidence: 89%

“…The biomarkers for cancer stem cells (CSCs) were expressed in this cluster. Such biomarkers as STMN1 [31,32], UBE2C [33] and PTTG1 [34] [35] were associated with tumor cell survival, clonality and tumorigenicity in several malignancies. This subcluster was regarded as stem tumor cells (sTCs, mTCs-C4-STMN1).…”

Section: Transcriptomic Tumor Heterogeneity Of Tumor Cells In Chordomamentioning

confidence: 99%

See 1 more Smart Citation

Single-cell transcriptome profiling reveals intra-tumoral heterogeneity in human chordomas

Duan

Zhang

et al. 2022

Cancer Immunol Immunother

View full text Add to dashboard Cite

Background: Chordoma is a rare and aggressive bone tumor with high recurrence. The intra-tumoral heterogeneity of chordomas is poorly understood, limiting the development of effective therapeutic strategies.Methods: Single-cell RNA sequencing was performed to delineate the transcriptomic landscape of chordomas. Six tumor samples of pathologically classical chordomas were obtained, and 33,737 cells that passed quality control were included in the analysis.Results: The main cellular populations identi ed with speci c markers were: chordomas cells (6392, 47.6%), broblasts (6945, 20.6%), mononuclear phagocytes (4734, 14.0%), and T/NK cells (3944, 11.7%). Downstream analysis was performed according to each cellular population. There were six subclusters of chordomas, which exhibited properties of an epithelial-like extracellular matrix, and stem cells with immunosuppression. Although few immune checkpoint was detected on cytotoxic immune cells such as T and NK cells, there was strong immunosuppression exerted by Tregs and M2 macrophages. In addition, the cellular interactions indicated an enhanced TGF-β signaling pathway as the main mechanism for tumor progression, invasion, and immunosuppression in chordomas.Conclusion: Our study contribute to the clari cation of intra-tumoral heterogeneity, and may pave the way to identify potential therapeutic targets in chordomas.

show abstract

Section: Discussionmentioning

confidence: 89%

Section: Transcriptomic Tumor Heterogeneity Of Tumor Cells In Chordomamentioning

confidence: 99%

Single-cell transcriptome profiling reveals intra-tumoral heterogeneity in human chordomas

Duan

Zhang

et al. 2022

Cancer Immunol Immunother

View full text Add to dashboard Cite

show abstract

“…PTTG1 plays an important role in a variety of malignant tumors ( 29 – 31 ). A recent study revealed that PTTG1 acts as a marker of tumor stem cells and regulates tumor stem cells, germline and stem cell-related genes and the malignant progression of ovarian tumors by affecting the self-renewal and epithelial-mesenchymal transformation ability of tumor stem cells ( 32 ). In addition, PTTG1 protein expression was found to be significantly higher in colorectal cancer tissues and cell lines ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑374c‑5p regulates PTTG1 and inhibits cell growth and metastasis in hepatocellular carcinoma by regulating epithelial‑mesenchymal transition

Xiog

Wang

et al. 2022

Mol Med Rep

View full text Add to dashboard Cite

a large number of studies have reported that microrna (mir)-374c-5p plays an important role in the occurrence and development of malignant tumors, but there is no research on the role of mir-374c-5p in hepatocellular carcinoma (Hcc). The aim of the present study was to investigate the role of mir-374c-5p in Hcc and the underlying molecular mechanism. The expression of mir-374c-5p in Hcc tissues and Hcc cell lines was analyzed via reverse transcription-quantitative Pcr. The association between mir-374c-5p and clinical pathology was also analyzed in patients with Hcc. Kaplan-Meier analysis and cox multivariate analysis were used to evaluate the prognostic significance of miR-374c-5p in Hcc. The biological functions of mir-374c-5p, including cell proliferation, migration and invasion and its potential molecular mechanism were analyzed in vivo and in vitro. in addition, the molecular mechanism of mir-374c-5p in Hcc was further explored. The results demonstrated that mir-374c-5p expression was lower in Hcc than in matched adjacent tissue samples. Patients with low expression of mir-374c-5p had poor prognosis and short survival time. overexpression of mir-374c-5p inhibited Hcc cell proliferation, migration and invasion in vitro. In vivo, it was found that overexpression of miR-374c-5p significantly inhibited the growth and proliferation of HCC cells. Dual-luciferase reporter assays verified that mir-374c-5p directly targets the 3'-untranslated region of pituitary tumor-transforming 1 (PTTG1) and regulates PTTG1 expression. in general, it was revealed that mir-374c-5p regulates the malignant biological behavior of Hcc through PTTG1, thereby affecting epithelial-mesenchymal transition. Thus, mir-374c-5p is a potential biological indicator to predict poor prognosis in patients with Hcc.

show abstract

“…Protein interaction analysis showed that there were 35 nodal proteins upregulated after SPINK13 treatment, of which 14 proteins were related to tumor. They were HIST2H2BE, HIST1H2AC, RCC1, CKS1B, UBE2C, TOP2A, CCNB2, CCNA2, CDC20, AURKB, PTTG1, BUBI, NEK2 and INCENP (30)(31)(32)(33)(34). Except that RCC1, AURKB, NEk2, and INCENP were not found in the KEGG pathway, the remaining 10 genes had the largest number in the cell cycle pathway.…”

Section: Protein Interaction Analysis Of Degsmentioning

confidence: 99%

Transcriptome analysis of the effect of a novel human serine protease inhibitor SPINK13 on gene expression in MHCC97-H cells

Wei¹,

An²,

An³

et al. 2021

Transl Cancer Res TCR

View full text Add to dashboard Cite

Background Serine peptidase inhibitor, Kazal type 13 (SPINK13) (also known as hespinter) is a low-molecular-weight inhibitor of uPA that was discovered in 2006. It was detected in prokaryotic cells in 2013 for the first time and preliminarily shown to inhibit hepG2 liver cancer cells growth in vitro in 2015. In this study, the differentially transcribed genes of MHCC97-H cells caused by SPINK13 treatment were studied by transcriptomics and the molecular mechanism of SPINK13 suppressing tumor cells was proposed using bioinformatics. Methods Preliminary study of the molecular mechanism of SPINK13’s anti-cancer effect was performed by identifying potential target sites and signal pathways of SPINK13 through transcriptomics and bioinformatics analysis. Results The results of the transcriptome study showed that there were 446 significantly differentially expressed genes between the experimental group and the blank control group, of which 347 genes were up-regulated and 99 genes were down-regulated. The Gene Ontology (GO) analysis showed that differentially expressed genes were enriched in cell growth regulation and cell division. They were enriched in the signal pathways of tumor transcription and cell cycle by Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis; there were 6 classical tumor signaling pathways (P<0.001): MAPK, apoptosis, tumor necrosis factor (TNF), cell cycle, p53, and transcriptional misregulation in cancer. There were 8 genes in 2 or more classical tumor signaling pathways at the same time: JUN , GADD45A , GADD45B , TNFRSF1A , FOS , CDKN1B , NFKBIA , and BBC3 . The interaction analysis of the proteins encoded by the differentially expressed genes showed that there were 35 interaction nodes in the up-regulated genes and 2 interaction nodes in the down-regulated genes. Conclusions This study showed that SPINK13 inhibits hepatocellular carcinoma cell development by regulating the JNK, p53, and the IKK/NF-κB pathways, its potential targets for antitumor drugs may be J UN , GADD45A , GADD45B , TNFRSF1A , FOS , CDKN1B , NFKBIA , and BBC3 .

show abstract

PTTG1: a Unique Regulator of Stem/Cancer Stem Cells in the Ovary and Ovarian Cancer

Cited by 19 publications

References 84 publications

Single-cell transcriptome profiling reveals intra-tumoral heterogeneity in human chordomas

Single-cell transcriptome profiling reveals intra-tumoral heterogeneity in human chordomas

miR‑374c‑5p regulates PTTG1 and inhibits cell growth and metastasis in hepatocellular carcinoma by regulating epithelial‑mesenchymal transition

Transcriptome analysis of the effect of a novel human serine protease inhibitor SPINK13 on gene expression in MHCC97-H cells

Contact Info

Product

Resources

About