DHRS2 inhibits cell growth and motility in esophageal squamous cell carcinoma

Zhou, Yun; Wang, L.; Ban, Xiaohua; Zeng, Tingting; Zhu, Ying; Li, M.; Guan, Xin Yuan; Li, Y.

doi:10.1038/onc.2017.383

Cited by 41 publications

(33 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HEP27 protein interacts with MDM2, which is a negative regulator of p53, resulting in p53 stabilization and induction of p53 transcriptional target genes (46). More recently, downregulation of DHRS2 was reported in ESCC tissues and its downregulation was associated with ESCC aggressiveness and clinical staging (47). Thus, that report arrived at the opposite conclusions from those in our study.…”

Section: Discussioncontrasting

confidence: 96%

Molecular pathogenesis of esophageal squamous cell carcinoma: Identification of the antitumor effects of miR‑145‑3p on gene regulation

et al. 2018

View full text Add to dashboard Cite

Although miR-145-5p (the guide strand of the miR-145 duplex) is established as a tumor suppressive microRNA (miRNA or miR), the functional significance of miR-145-3p (the passenger strand of the miR-145 duplex) in cancer cells and its targets remains obscure. In our continuing analysis of esophageal squamous cell carcinoma (ESCC) pathogenesis, the aim of the present study was to identify important oncogenes and proteins that are controlled by miR-145-3p. Overexpression of miR-145-3p significantly reduced cancer cell proliferation, migration and invasive abilities, and further increased apoptotic abilities. In ESCC cells, 30 possible oncogenic targets were identified that might be regulated by miR-145-3p. Among these targets, dehydrogenase/reductase member 2 (DHRS2) and myosin IB (MYO1B) were focused on to investigate their functional roles in ESCC cells. DHRS2 and MYO1B were directly regulated by miR-145-3p in ESCC cells by dual luciferase reporter assays. Aberrantly expressed DHRS2 and MYOIB were detected in ESCC clinical specimens, and their overexpression enhanced cancer cell aggressiveness. Genes regulated by antitumor miR-145-3p were closely associated with the molecular pathogenesis of ESCC. The approach based on antitumor miRNAs may contribute to the understanding of ESCC molecular pathogenesis.

show abstract

Section: Discussioncontrasting

confidence: 96%

Molecular pathogenesis of esophageal squamous cell carcinoma: Identification of the antitumor effects of miR‑145‑3p on gene regulation

et al. 2018

View full text Add to dashboard Cite

show abstract

“…4B and C). DHRS2 is reported to stabilize p53 levels via Ser15 phosphorylation in esophageal squamous-cell carcinoma cells (Zhou et al, 2018). However, we observed no changes in p53…”

Section: Internal Synthesis Of Polyp Leads To Downregulation Of the Dcontrasting

confidence: 78%

“…One such example is DHRS2, which showed drastic changes in mRNA levels and was completely undetected in all five Ppk1 biological replicates. DHRS2 protein downregulation via shRNA was previously shown to decrease p53 phosphorylation at Ser15 (Zhou et al, 2018). We observed no significant change in phosphorylated p53 (Ser15) levels accompanying polyP-induced DHRS2 downregulation.…”

Section: Discussioncontrasting

confidence: 59%

A broad response to intracellular long-chain polyphosphate in human cells

Bondy‐Chorney

Abramchuk

Nasser

et al. 2020

Preprint

View full text Add to dashboard Cite

Polyphosphates (PolyP) are composed of long chains of inorganic phosphates linked together by phosphoanhydride bonds. They are found in all kingdoms of life, playing roles in cell growth, infection, and blood coagulation. A resurgence in interest in polyP has shown links to diverse aspects of human disease. However, unlike in bacteria and lower eukaryotes, the mammalian enzymes responsible for polyP metabolism are not known. Many studies have resorted to adding polyP to cell culture media, but it is not clear if externally applied polyP enters the cell to impact signaling events or whether their effect is mediated exclusively by extracellular receptors. For the first time, we use RNA-seq and mass spectrometry to define a broad impact of polyP produced inside of mammalian cells via ectopic expression of the E. coli polyP synthetase Ppk1. RNA-seq demonstrates that Ppk1 expression impacts expression of over 350 genes enriched for processes related to transcription and cell motility. Analysis of proteins via label-free mass spectrometry identified over 100 changes with functional enrichment in cell migration. Follow up work suggests a role for internally-synthesized polyP in promoting activation of mTOR and ERK1/2-EGR1 signaling pathways implicated in cell growth and stress. Finally, fractionation analysis shows that polyP accumulated in multiple cellular compartments and was associated with the relocalization several nuclear/cytoskeleton proteins, including chromatin bound proteins DEK, TAF10, GTF2I and translation initiation factor eIF5b. Our work is the first to demonstrate that internally produced polyP can activate diverse signaling pathways in human cells.Significance StatementFor many years following its discovery in 1890, polyphosphates (polyP) were dismissed as evolutionary fossils. Best understood for its role in bacteria and yeast, our understanding of polyP in mammals remains rudimentary because the enzymes that synthesize and degrade polyP in mammalian systems are currently unknown. In our work, we carried out large-scale transcriptome and proteome approaches on human cells designed to accumulate internally produced polyP via ectopic expression of a bacterial polyP synthetase. Our work is the first to systematically assess the impact of increased intracellular polyP.

show abstract

“…Moreover, double homeobox A pseudogene 10, located in chr14q11.2, promotes an aggressive phenotype by binding lysine-specific histone demethylase 1 and repressing large tumor suppressor kinase 2 and Ras-related glycolysis inhibitor and calcium channel regulator expression levels in NSCLC (17). Furthermore, previous studies have revealed that chr14q11.2 may participate in cancer development (18)(19)(20).…”

Section: Discussionmentioning

confidence: 99%

Epididymal protein 3A is upregulated and promotes cell proliferation in non‑small cell lung cancer

Xing

Pan

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

Lung cancer is one of the most common cancer types and a major contributor to cancer-associated mortalities worldwide. The aim of the present study was to investigate the function of the epididymal protein 3A (EDDM3A) in non-small cell lung cancer (NSCLC). Data from patients with NSCLC were retrieved from The Cancer Genome Atlas and analyzed, and the differences in EDDM3A expression level between 30 NSCLC tissues and matched adjacent non-tumor tissues (>5 cm) were assessed via tissue microarray analysis. It was revealed that, compared with adjacent non-tumor tissues, EDDM3A expression was significantly increased in NSCLC tissues (P=4.19x10-2). To knock down EDDM3A expression in a human NSCLC cell line, lentivirus-mediated short hairpin RNAs (shRNAs) were used, and the knockdown efficiency was assessed via reverse transcription-quantitative PCR and western blotting. Moreover, cell proliferation was evaluated with an MTT assay and Celigo imaging cytometry. In addition, cell apoptosis was detected by Annexin V staining. It was demonstrated that knockdown of EDDM3A inhibited the proliferation of A549 cells. Furthermore, compared with the control group, the apoptotic rate of the EDDM3A-shRNA group was significantly higher. Collectively, the present results indicate the potential role of EDDM3A in NSCL and suggest that EDDM3A may represent a potent therapeutic target for treating patients with NSCLC.

show abstract

DHRS2 inhibits cell growth and motility in esophageal squamous cell carcinoma

Cited by 41 publications

References 37 publications

Molecular pathogenesis of esophageal squamous cell carcinoma: Identification of the antitumor effects of miR‑145‑3p on gene regulation

Molecular pathogenesis of esophageal squamous cell carcinoma: Identification of the antitumor effects of miR‑145‑3p on gene regulation

A broad response to intracellular long-chain polyphosphate in human cells

Epididymal protein 3A is upregulated and promotes cell proliferation in non‑small cell lung cancer

Contact Info

Product

Resources

About