Category Archives: Intestinal Cell

Intestinal Cell News is an online publication and email newsletter that curates the latest research using intestinal cells.
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Since 2015, Intestinal Cell News has been a valuable resource for keeping researchers and medical professionals updated on the latest publications, news and events in the field of gastrointestinal cell biology. Our editorial team collects and publishes the most current articles and reviews using stomach, colon, and small and large intestinal cells. We cover topics including the culturing of intestinal cells, intestinal organoids, intestinal cancers, and gastrointestinal conditions such as irritable bowel syndrome and Crohn’s disease.

Regenerative Reprogramming of the Intestinal Stem Cell State via Hippo Signaling Suppresses Metastatic Colorectal Cancer

The authors demonstrated that the Hippo kinases LATS1/2 and MST1/2, which inhibited YAP activity, were required for maintaining Wnt signaling and canonical stem cell function.
[Cell Stem Cell]
Cheung, P., Xiol, J., Dill, M. T., Yuan, W.-C., Panero, R., Roper, J., Osorio, F. G., Maglic, D., Li, Q., Gurung, B., Calogero, R. A., Yilmaz, Ö. H., Mao, J., & Camargo, F. D. (2020). Regenerative Reprogramming of the Intestinal Stem Cell State via Hippo Signaling Suppresses Metastatic Colorectal Cancer. Cell Stem Cell, 0(0). https://doi.org/10.1016/j.stem.2020.07.003 Cite
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LIF Is Essential for ISC Function and Protects against Radiation-Induced Gastrointestinal Syndrome

Leukemia inhibitory factor (LIF) is a cytokine essential for maintaining pluripotency of mouse ESCs. Scientists found that LIF was present in the intestinal stem cell (ISC) niche in crypts and critical for the function of ISCs in maintaining the intestinal epithelial homeostasis and regeneration.
[Cell Death & Disease]
Wang, H., Wang, J., Zhao, Y., Zhang, X., Liu, J., Zhang, C., Haffty, B., Verzi, M., Zhang, L., Gao, N., Feng, Z., & Hu, W. (2020). LIF is essential for ISC function and protects against radiation-induced gastrointestinal syndrome. Cell Death & Disease, 11(7), 1–15. https://doi.org/10.1038/s41419-020-02790-6 Cite
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miR-3622a-3p Acts as a Tumor Suppressor in Colorectal Cancer by Reducing Stemness Features and EMT through Targeting Spalt-Like Transcription Factor 4

The effect of miR-3622a-3p on proliferation, apoptosis, cell cycle, migration and invasion of colorectal cancer (CRC) cells were investigated by a series of biological function assays and the results revealed that miR-3622a-3p could inhibit the malignant biological properties of CRC.
[Cell Death & Disease]
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Upregulation of OSBPL3 by HIF1A Promotes Colorectal Cancer Progression through Activation of RAS Signaling Pathway

Scientists investigated the role of oxysterol-binding protein like protein 3 in colorectal cancer and found that its expression was significantly higher in colorectal cancer tissues than that in normal tissues.
[Cell Death & Disease]
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Pevonedistat (MLN4924): Mechanism of Cell Death Induction and Therapeutic Potential in Colorectal Cancer

Investigators identified p53 as an important mediator of the apoptotic response to pevonedistat. They also found roles for the extrinsic and intrinsic apoptotic pathways in mediating the apoptotic effects of pevonedistat in colorectal cancer cells, as well as a role for BID, which modulates a cross-talk between these pathways.
[Cell Death Discovery]
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The LIM Protein Ajuba Augments Tumor Metastasis in Colon Cancer

The authors found that cells depleted of Ajuba were less proliferative, more sensitive to irradiation, migrated less and less efficient in colony formation. In addition, loss of Ajuba expression decreased the tumor burden in a murine model of colorectal metastasis to the liver.
[Cancers]
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LintonPharm Announces Authorization From China Health Authority to Proceed With a Global Phase III Trial Evaluating Catumaxomab in Advanced Gastric Cancer

LintonPharm Co. Ltd. announced that China National Medical Products Administration (NMPA) authorized the company to proceed with a Phase III trial for catumaxomab in patients with peritoneal carcinomatosis, a form of advanced gastric cancer that has spread to the tissue that lines the abdominal cavity.
[LintonPharm]
Press Release

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Nitric Oxide (NO) and NO Synthases (NOS)-Based Targeted Therapy for Colon Cancer

The authors summarize the multifaceted mechanisms of nitric oxide (NO) -mediated networks in several hallmarks of colorectal cancer. Also, the authors review the clinical manifestation and limitations of NO donors and NO synthase (NOS) inhibitors in clinical trials and discuss the possible directions of NO/NOS therapies in the immediate future.
[Cancers]
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Circular RNA circCTNNA1 Promotes Colorectal Cancer Progression by Sponging miR-149-5p and Regulating FOXM1 Expression

circCTNNA1 promoted colon cancer cell proliferation, migration, and invasion in vitro and in vivo. It could serve as a competing endogenous RNA of miR-149-5p to counteract the suppressive effect of miR-149-5p on downstream target Forkhead Box M1.
[Cell Death & Disease]
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LASP1 Interacts with N-WASP to Activate the Arp2/3 Complex and Facilitate Colorectal Cancer Metastasis by Increasing Tumour Budding and Worsening the Pattern of Invasion

Investigators suggested a new mechanism for LIM and SH3 protein 1(LASP1)-mediated colorectal cancer metastasis determined by exploring LASP1-interacting proteins, and identified N–Wiskott–Aldrich syndrome protein as a potential therapeutic target for colorectal cancer.
[Oncogene]
Abstract

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PI3K-Targeting Strategy Using Alpelisib to Enhance the Antitumor Effect of Paclitaxel in Human Gastric Cancer

The authors investigated the anti-tumor effects of alpelisib, a PI3K p110α-specific inhibitor, using preclinical models of gastric cancer. The combined effects of alpelisib and paclitaxel on gastric cancer was also evaluated.
[Scientific Reports]
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Copper Bioavailability Is a KRAS-Specific Vulnerability in Colorectal Cancer

ATP7A regulates the intracellular copper levels and tumor growth in KRAS-transformed cells. Investigators demonstrated that inhibiting Copper supply was an attractive therapeutic option for KRAS-mutant cells.
[Nature Communications]
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