Researchers performed Affymetrix Gene Chip miRNA 4.0 microarray and observed differential regulation of miRNAs (75 upregulated and 199 downregulated) in metastatic MDA-MB-231 cells as compared to immortalized human non-tumorigenic breast epithelial cells.
Scientists uncovered that estrogen receptor-positive breast cancer cells cultured within extracellular matrix -scaffolds had an increase in ER signaling that occured via a MAPK-dependent, but estrogen-independent manner.
[Molecular Cancer Research]
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Tim-3 was overexpressed in vascular endothelial HMVECs and HUVECs and in vitro assays were used to determine that Tim-3 promoted cell proliferation, migration, invasion and tube formation through activating cyclin D1, Ras homolog gene family member A and vascular endothelial growth factor receptor 2.
The loss of SNAI2 in cancer-associated fibroblasts limited the production of some cytokines, which influenced AKT/ERK tumor signaling and subsequent proliferative and metastatic capacity of ERBB2+ breast cancer cells.
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Blanco-Gómez, A., Hontecillas-Prieto, L., Corchado-Cobos, R., García-Sancha, N., Salvador, N., Castellanos-Martín, A., Sáez-Freire, M. del M., Mendiburu-Eliçabe, M., Alonso-López, D., Rivas, J. D. L., Lorente, M., García-Casas, A., Carmen, S. D., Abad-Hernández, M. del M., Cruz-Hernández, J. J., Rodríguez-Sánchez, C. A., Claros-Ampuero, J., García-Cenador, B., García-Criado, J., … Castillo-Lluva, S. (2020). Stromal SNAI2 is required for ERBB2 breast cancer progression. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-0278 Cite
The cytotoxic effect of diltiazem, gemcitabine, and 5-fluorouracil in single and combined forms against PANC-1 and AsPC-1 cells were assayed by MTT. Flow cytometric analysis was used for the determination of cell cycle, apoptosis, and stemness markers in pancreatic cancer cells.
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El-Mahdy, H. A., El-Husseiny, A. A., Kandil, Y. I., & Gamal El-Din, A. M. (2020). Diltiazem potentiates the cytotoxicity of gemcitabine and 5-fluorouracil in PANC-1 human pancreatic cancer cells through inhibition of P-glycoprotein. Life Sciences, 118518. https://doi.org/10.1016/j.lfs.2020.118518 Cite
A1874-induced degradation of BRD4 protein and downregulated BRD-dependent genes in colon cancer cells. A1874-induced anti-colon cancer cell activity was more potent than the known BRD4 inhibitors. In BRD4-knockout colon cancer cells A1874 remained cytotoxic, indicating the existence of BRD4-independent mechanisms.
[Cell Death & Disease]
The expression of m6A associated enzymes and total m6A level were measured by Western Blotting analysis and m6A RNA Methylation Quantification Kit respectively. Cell cycle was analyzed by flowcytometry. The interaction of IGF2BP3 and related targets was analyzed by RNA immunoprecipitation and m6A RNA immunoprecipitation assays.
[Journal of Experimental & Clinical Cancer Research]
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Researchers showed that fibroblast growth factor receptor 3 (FGFR3) inactivation accelerated bone marrow suppression-induced hematopoietic stem and progenitor cell expansion by upregulating FGFR1 and its downstream transcriptional factor, ELK, which regulates the expression of Cyclin D1 gene at the level of transcription.
[Biology of Blood and Marrow Transplantation]
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Colony formation assay and flow cytometry were used to evaluate the effect of garcinone C on the proliferation and cell cycle progression of colon cancer cells.
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RelB promoted breast cancer cell proliferation through increased G1/S transition and/or decreased apoptosis by upregulation of Cyclin D1 and Bcl-2. RelB upregulated bone metastatic protein MMP1 expression through binding to an NF-κB enhancer element located at the 5′-flanking region.
[Cell Communication and Signaling]
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Wang, M., Zhang, Y., Xu, Z., Qian, P., Sun, W., Wang, X., Jian, Z., Xia, T., Xu, Y., & Tang, J. (2020). RelB sustains endocrine resistant malignancy: an insight of noncanonical NF-κB pathway into breast Cancer progression. Cell Communication and Signaling, 18(1), 128. https://doi.org/10.1186/s12964-020-00613-x Cite
Scientists investigated a direct role of Yap in constitutive androstane receptor (CAR)‐driven hepatomegaly and hepatocyte proliferation using hepatocyte‐specific Yap‐KO mice. AAV8‐TBG‐CRE vector was injected to Yap‐floxed mice for achieving hepatocyte‐specific Yap deletion followed by TCPOBOP‐treatment.
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Bhushan, B., Molina, L., Koral, K., Stoops, J. W., Mars, W. M., Banerjee, S., Orr, A., Paranjpe, S., Monga, S. P., Locker, J., & Michalopoulos, G. K. (n.d.). Yap is crucial for CAR-driven hepatocyte proliferation, but not for induction of drug metabolism genes in mice. Hepatology, n/a(n/a). https://doi.org/10.1002/hep.31521 Cite