Investigators found that SMAD2 was highly expressed in hepatocellular carcinoma (HCC) and elevated SMAD2 expression predicted shorter overall survival time for HCC patients. SMAD2 promoted mobility and proliferation of HCC cells in vitro.
[Journal of Experimental & Clinical Cancer Research]
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Huang, Z., Wen, J., Yu, J., Liao, J., Liu, S., Cai, N., Liang, H., Chen, X., Ding, Z., & Zhang, B. (2020). MicroRNA-148a-3p inhibits progression of hepatocelluar carcimoma by repressing SMAD2 expression in an Ago2 dependent manner. Journal of Experimental & Clinical Cancer Research, 39(1), 150. https://doi.org/10.1186/s13046-020-01649-0 Cite
Brain organoids derived from iPSCs of patients are a powerful avenue to investigate the pathophysiological processes. Scientists generated iPSC-derived cerebral organoids from monozygotic twins discordant for psychosis.
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Sawada, T., Chater, T. E., Sasagawa, Y., Yoshimura, M., Fujimori-Tonou, N., Tanaka, K., Benjamin, K. J. M., Paquola, A. C. M., Erwin, J. A., Goda, Y., Nikaido, I., & Kato, T. (2020). Developmental excitation-inhibition imbalance underlying psychoses revealed by single-cell analyses of discordant twins-derived cerebral organoids. Molecular Psychiatry, 1–17. https://doi.org/10.1038/s41380-020-0844-z Cite
Loss of function studies of PIAS1 and TIF1γ suggested that these E3 ligases act in an interdependent manner to suppress epithelial–mesenchymal transition of breast cell-derived tissue organoids. The authors unveiled a novel mechanism by which SUMO E3 ligases coordinate substrate SUMOylation with biological implications.
[Cell Death & Differentiation]
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Scientists found that deletion of Erk1/2 in intestinal epithelial cells at embryonic stages resulted in an unexpected increase in cell proliferation and migration, expansion of intestinal stem cells and formation of polyp-like structures, leading to postnatal death.
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ERK/MAPK signaling is essential for intestinal development through Wnt pathway modulation | Development. (n.d.). Retrieved August 7, 2020, from https://dev.biologists.org/content/early/2020/07/30/dev.185678 Cite
Researchers found that STK4 knockdown enhanced sphere formation and metastasis in vitro and promoted tumor development in vivo. STK4 colocalized with β‐catenin and directly phosphorylated β‐catenin resulting to its degradation via the ubiquitin‐mediated pathway.
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Lin, C.-H., Hsu, T.-I., Chiou, P.-Y., Hsiao, M., Wang, W.-C., Chen, Y.-C., Lin, J.-T., Wang, J.-Y., Lin, P.-C., Lin, F.-C., Tseng, Y.-K., Cheng, H.-C., Chen, C.-L., & Lu, P.-J. (n.d.). Downregulation of STK4 promotes colon cancer invasion/migration through blocking β-catenin degradation. Molecular Oncology, n/a(n/a). https://doi.org/10.1002/1878-0261.12771 Cite
Investigators surveyed the expression levels and clinical significance of novel long noncoding RNAs related to CYP24A1 and PFDN4 genes in colorectal cancer using real‐time polymerase chain reaction. They also assessed the expression of these genes after vitamin D treatment in HCT‐116 and HT‐29 colon cancer cell lines.
[Journal of Cellular Physiology]
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Sadeghi, H., Nazemalhosseini‐Mojarad, E., Sahebi, U., Fazeli, E., Azizi‐Tabesh, G., Yassaee, V. R., Savabkar, S., Aghdaei, H. A., Zali, M. R., & Mirfakhraie, R. (n.d.). Novel long noncoding RNAs upregulation may have synergistic effects on the CYP24A1 and PFDN4 biomarker role in human colorectal cancer. Journal of Cellular Physiology, n/a(n/a). https://doi.org/10.1002/jcp.29992 Cite
In the wound healing assay, berberine exhibited the ability to promote cell migration, indicating that berberine could probably recover the function of intestinal epithelial cells when the intestinal epithelial barrier was damaged by the peritoneal dialysis fluid.
[Journal of Ethnopharmacology]
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Zhang, D., Jiang, L., Wang, M., Jin, M., Zhang, X., Liu, D., Wang, Z., Yang, L., & Xu, X. (2020). Berberine inhibits intestinal epithelial barrier dysfunction in colon caused by peritoneal dialysis fluid by improving cell migration. Journal of Ethnopharmacology, 113206. https://doi.org/10.1016/j.jep.2020.113206 Cite
Intestinal organoids were grown from rectal biopsies in a cohort of 97 subjects with cystic fibrosis. Residual CFTR function was measured by quantifying organoid swelling induced by forskolin and response to modulators by quantifying organoid swelling induced by CFTR correctors, potentiator and their combination.
[European Respiratory Journal]
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Ramalho, A. S., Fürstová, E., Vonk, A. M., Ferrante, M., Verfaillie, C., Dupont, L., Boon, M., Proesmans, M., Beekman, J. M., Sarouk, I., Cordero, C. V., Vermeulen, F., & Boeck, K. D. (2020). Correction of CFTR function in intestinal organoids to guide treatment of Cystic Fibrosis. European Respiratory Journal. https://doi.org/10.1183/13993003.02426-2019 Cite
The three dihydroxystilbenes in this study inhibited colon carcinogenesis and tumor growth as well as increases in colon IL-1β, IL-6, MCP-1, and PD-1 levels in AOM/DDS-treated mice in vivo. The three dihydroxystilbenes also suppressed COX-2 expression in colon tumors in vivo and inhibited PD-1 elevations in M2-THP-1 macrophages in vitro.
[European Journal of Pharmacology]
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Kimura, Y., Sumiyoshi, M., Kiyoi, T., & Baba, K. (2020). Dihydroxystilbenes prevent azoxymethane/dextran sulfate sodium-induced colon cancer by inhibiting colon cytokines, a chemokine, and programmed cell death-1 in C57BL/6J mice. European Journal of Pharmacology, 173445. https://doi.org/10.1016/j.ejphar.2020.173445 Cite
Mice lacking intestinal TLR9 had profoundly increased liver injury after hepatic ischemia reperfusion(IR) compared to WT mice with exacerbated hepatocyte necrosis, apoptosis, neutrophil infiltration, and inflammatory cytokine generation. They also observed increased small intestinal inflammation and apoptosis after hepatic IR in intestinal TLR9 deficient mice. Fecal short‐chain fatty acids butyrate and propionate levels were lower in intestinal TLR9 deficient mice.
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MIR503HG negatively regulated its target miR-107. MiR-107 overexpression reversed the anti-tumor effects of MIR503HG overexpression on colon cancer cells. Par4 was a target of miR-107, which was positively regulated by MIR503HG. The promoting effects of MIR503HG silencing on colon cancer cells were eliminated by Par4 overexpression.
[Experimental Cell Research]
Y-27632 induced the acquisition of a pro-migratory cell phenotype and increased cancer cell invasiveness in both 3- and 2-dimensions assays. This effect was prevented by the inhibition of NaV1.5 voltage-gated sodium channel activity. ROCK inhibition enhanced the activity of the pro-invasive NaV1.5 channel through a pathway that was independent of gene expression regulation.
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Poisson, L., Lopez-Charcas, O., Chadet, S., Bon, E., Lemoine, R., Brisson, L., Ouaissi, M., Baron, C., Besson, P., Roger, S., & Moussata, D. (2020). Rock inhibition promotes Na V 1.5 sodium channel-dependent SW620 colon cancer cell invasiveness. Scientific Reports, 10(1), 13350. https://doi.org/10.1038/s41598-020-70378-3 Cite