Cancer Stem Cell News Volume 7.28 | Jul 18 2018

TOP STORY

A Novel TGF-β and H19 Signaling Axis in Tumor-Initiating Hepatocytes That Regulates Hepatic Carcinogenesis

Scientists revealed that treatment of cultured tumor-initiating hepatocytes (TICs) with TGF‐β inhibited the expression of progenitor cell factors. They identified H19 as one of the most upregulated long noncoding RNA in association with TGF‐β receptor II (Tgfbr2) inactivation in TICs. Tgfbr2 inactivation by Ad‐Cre led to a 5‐fold increase of H19 expression in TICs. TGF‐β treatment reduced H19 expression. [Hepatology] Abstract

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Fatal Correlation between YAP1 Expression and Glioma Aggressiveness: Clinical and Molecular Evidence

Using patient‐derived glioblastoma stem cell cultures, investigators demonstrated that YAP1 was activated and it controlled cell proliferation. Transcriptome analysis revealed lower expression of YAP1 in the proneural GBM subtype. Overexpression of YAP1 was sufficient to inhibit the OLIG2 proneural marker suggesting its involvement in maintenance of GBM phenotype. [J Pathol] Abstract

GATA3 as a Master Regulator and Therapeutic Target in Ovarian High-Grade Serous Carcinoma Stem Cells

GATA3 expression associated with poor prognosis of ovarian high‐grade serous carcinoma (HGSC) patients, and was found to recruit the histone H3, lysine 27 demethylase, UTX, activate stemness markers, and promote stem‐like phenotypes in ovarian HGSC cell lines. Targeting UTX by its inhibitor, GSKJ4, impeded GATA3‐driven stemness phenotypes, and enhanced apoptosis of GATA3‐expressing cancer cells. [Int J Cancer] Abstract

Regorafenib Suppresses Colon Tumorigenesis and the Generation of Drug Resistant Cancer Stem-Like Cells via Modulation of miR-34a Associated Signaling

Scientists showed that regorafenib treatment decreased the stemness phenotypes including tumor sphere formation, and side-population, of both HCT-116R and DLD-1R cells. Additionally, regorafenib suppressed the cell viability in both cell lines synergistically with 5-FU. Regorafenib-mediated effects were associated with the induction of tumor suppressor miR-34a and suppression of WNT/β-catenin signaling. [J Exp Clin Cancer Res] Full Article

Tescalcin/C-Src/IGF1Rβ-Mediated STAT3 Activation Enhances Cancer Stemness and Radioresistant Properties through ALDH1

Tescalcin (TESC) expression and the phosphorylation of signal transducer and activator of transcription 3 (STAT3) were upregulated in cancer stem cell-like ALDH1^high cells than in ALDH1^low cells sorted from A549 non-small cell lung cancer cells. TESC activated insulin-like growth factor 1 receptor (IGF1R) by the direct recruitment of proto-oncogene tyrosine kinase c-Src to IGF1Rβ complex. [Sci Rep] Full Article

VEGFC/VEGFR3 Axis Mediates TGFβ1-Induced Epithelial-to-Mesenchymal Transition in Non-small Cell Lung Cancer Cells

Transforming growth factor β1 (TGFβ1) treatment resulted in a significant epithelial-mesenchymal transition morphological change in TGFβ1-sensitive non-small cell lung cancer (NSCLC) cells but not in insensitive cells. TGFβ1 was able to enhance the mRNA expression of Oct4, Nanog and Sox2 and drastically increased anchorage-independent colony formation in TGFβ1-sensitive NSCLC cells, suggesting the acquisition of cancer stem-like properties. [PLoS One] Full Article

The Therapeutic Targeting of the FGFR1/Src/NF-κB Signaling Axis Inhibits Pancreatic Ductal Adenocarcinoma Stemness and Oncogenicity

Investigators showed that ALDH^high pancreatic cancer cells exhibited stem cell-like phenotype and expressed higher levels of FGFR1, Src, NF-κB, alongside stemness markers like Oct4 and Sox2, compared to their ALDH^low/null counterparts, suggesting the preferential activation of the FGFR1/Src/NF-κB signaling axis in pancreatic cancer stem cells. [Clin Exp Metastasis] Abstract | Graphical Abstract

Homeobox Containing 1 Inhibits Liver Cancer Progression by Promoting Autophagy as Well as Inhibiting Stemness and Immune Escape

Homeobox containing 1 (HMBOX1) increased the LC3 II/LC3 I ratio, the endogenous autophagy marker, and inhibited the p38/AKT/mTOR pathway. Cancer stem cell specific genes, including CD133, KLF4, ESG1 and SOX2, were significantly downregulated upon HMBOX1 overexpression. The susceptibility of HepG2 cells to NK cell‑mediated cytolysis was increased by HMBOX1 overexpression and weakened by siRNA-mediated inhibition of HMBOX1. [Oncol Rep] Abstract

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Perspective: Bidirectional Exosomal Transport between Cancer Stem Cells and Their Fibroblast-Rich Microenvironment during Metastasis Formation

The authors overview potential links between cancer stem cells and the exosome-mediated fibroblast-enriched metastatic niche formation to discuss their role in the promotion of tumor growth and metastatic expansion in breast carcinoma models. [Breast Cancer] Full Article

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University of Chicago Medicine Comprehensive Cancer Center Status Renewed

The National Cancer Institute, has renewed the University of Chicago Medicine Comprehensive Cancer Center’s designation as a comprehensive cancer center. The designation recognizes the center’s distinction as a center of research excellence in basic, clinical and population sciences, as well as a valued community and regional resource for cancer information, cancer education and cancer outreach. [The University of Chicago Medicine] Press Release

Israel Grants $33 Million to GE, Medtronic, Change Healthcare to Boost R&D

Three multinational companies have received an Israeli government grant of 120 million shekels ($33 million) aimed at boosting the presence of large companies and establishing Israel as a hub in biotechnology and medicine. [Reuters] Press Release

Leaky Pipeline for Women Scientists Dries Up after They Win First Big Grant

After they secure their first major research grant from the US National Institutes of Health, women are almost as successful as men at netting further awards from the agency, according to an analysis published in Proceedings of the National Academy of Sciences. [Nature News] Editorial

U.K. Votes to ‘Fully Participate’ in EMA after Brexit

British politicians have voted for the U.K. to try to remain close to the European Medicines Agency (EMA) after Brexit. The voted-for text tasks the government with seeking to secure the right for the U.K. to “fully participate” in the regional regulatory network after it leaves the European Union. [FierceBiotech] Editorial

A Top Chinese Brain Scientist Wonders How He Ended Up on the U.S. Visa Blacklist

Frustrated with a string of unexplained U.S visa denials, a top Chinese brain scientist has decided to go public, copying numerous journalists on an email to officials at the U.S Embassy in Beijing pleading his case. [ScienceInsider] Press Release

Cancer Geneticist Quits after Harassment Allegations

Following numerous allegations that she harassed fellow employees, Nazneen Rahman, a cancer geneticist at the Institute of Cancer Research in the U.K., will leave her post. Rahman had already been on administrative leave since last November. Dozens of colleagues signed a letter last year describing bullying by Rahman. [The Scientist] Editorial

NEW The 5^th Canadian Cancer Research Conference
November 3-5, 2019
Ottawa, Ontario, Canada

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NEW Postdoctoral Fellow – Cancer Research (The University of Texas MD Anderson Cancer Center)

Postdoctoral Scholar – Statistical Bioinformatics (The University of Iowa)

Postdoctoral Positions – Gene Regulation and/or Cancer Biology (University of North Carolina at Chapel Hill School of Medicine)

Postdoctoral Researcher – Cancer Stem Cells and Epitranscriptomics (University of California San Diego)

Postdoctoral Fellowship – Structure-Based Studies for a Search of New Drug Leads for Leukemia Treatment (European Molecular Biology Laboratory)

Postdoctoral Scientist – Drug Discovery & Cancer Stem Cell Biology (Cancer Research UK Manchester Institute)

Postdoctoral Fellow – Cancer Biology (Children’s Cancer Therapy Development Institute)

Tenure-Track Faculty Positions – Various (The Ohio State University)

Postdoctoral Fellow – Stem Cell Biology and Pharmacogenomics (Northwestern University Feinberg School of Medicine)

PhD Student – Cell Signaling (German Cancer Research Center)

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