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Condition: Polyps
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Total 44 results found since Jan 2013.
The siRNA-mediated knockdown of SNHG4 efficiently induced pro-apoptotic signaling and suppressed metastasis in SW1116 colorectal cancer cell line
CONCLUSIONS: In conclusion, SNHG4 promotes CRC by dysregulating apoptosis and cell migration, and shows significant prognostic potential for CRC.PMID:37715875 | DOI:10.1007/s11033-023-08742-5
Source: Mol Biol Cell - September 16, 2023 Category: Molecular Biology Authors: Mina Khajehdehi Mohammad Khalaj-Kondori Behzad Baradaran Source Type: research
Cancers, Vol. 15, Pages 4572: Tumor-Promoting Role of GNA14 in Colon Cancer Development
In this study, we examined the effect of GNA14 on CRC through genetic approaches in vitro and in vivo. We found that GNA14 knockdown by small interfering RNA (siRNA) inhibited the proliferation of CRC cells SW403 and HT29. Gna14 knockout mice developed normally without obvious abnormalities. However, the number of polyps in the small intestine was significantly reduced in Gna14 knockout mice compared to control mice after mating with ApcMin mice, a representative CRC mouse model. In particular, deletion of the Gna14 inhibited polyp growth, especially in the distal end of the small intestine. Histological examination showed...
Source: Cancers - September 15, 2023 Category: Cancer & Oncology Authors: Rahui Park Seungmin Lee Hyunjung Chin Anh Thai-Quynh Nguyen Daekee Lee Tags: Article Source Type: research
MiR-214 Expression Is Elevated in Chronic Rhinosinusitis Mucosa and Regulates Lipopolysaccharide-Mediated Responses in Undifferentiated Human Nasal Epithelial Cell Culture
CONCLUSION: Taken together, miR-214 regulates LPS-mediated inflammation and MUC5AC expression via targeting SIRT1, and STAT3/GDF15 may involve in the regulation of miR-214 inhibitor on inflammation and MUC5AC expression.PMID:36797977 | DOI:10.1177/19458924231152683
Source: American Journal of Rhinology and Allergy - February 17, 2023 Category: ENT & OMF Authors: Zhou Wang Dong Lin Yuxiang Zhao Hui Liu Ting Yang An Li Source Type: research
Increased CYR61 expression activates CCND1/c-Myc pathway to promote nasal epithelial cells proliferation in chronic rhinosinusitis with nasal polyps
CONCLUSIONS: CYR61, CCND1 and c-Myc were primarily expressed by epithelial cells in nasal mucosa. CYR61, CCND1 and c-Myc expression levels were increased in CRSwNP compared with controls. CYR61 could interact with ITGA2 to enhance HNEC proliferation via upregulating CCND1 and c-Myc levels in the HNEC, leading to hyperplastic nasal epithelium in CRSwNP.PMID:36681101 | DOI:10.1016/j.clim.2023.109235
Source: Clinical Immunology - January 21, 2023 Category: Allergy & Immunology Authors: Chunyu Luo Ying Zhu Jiayao Zhou Xiwen Sun Shiyao Zhang Shaolin Tan Zhipeng Li Hai Lin Weitian Zhang Source Type: research
Identification of a circRNA/miRNA/mRNA ceRNA Network as a Cell Cycle-Related Regulator for Chronic Sinusitis with Nasal Polyps
CONCLUSION: CeRNA networks including hsa_circ_0031594, hsa-miR-1260b, and NCAPG2, and hsa_circ_0031594, hsa-miR-6507-5p, and PRC1 may be key regulators for CRSwNP occurrence, and may be potential targets for the pathogenesis and treatment development of CRSwNP.PMID:35494315 | PMC:PMC9045834 | DOI:10.2147/JIR.S358387
Source: Cell Research - May 2, 2022 Category: Cytology Authors: Qi Sun Zhen Liu Xiangya Xu Yujuan Yang Xiao Han Cai Wang Fei Song Yakui Mou Yumei Li Xicheng Song Source Type: research
Late Breaking Abstract - Aldo-keto reductases expression correlate corticoids efficacy in vitro and on chronic rhinosinusitis with nasal polyps
Conclusion: AKR1C1, and possibly AKR1C2, seem to participate in the corticoid response by a non-catalytic mechanism, which may be related to GRα nuclear localization. Based on in vitro evidence, the high expression of AKR1C1 in CRSwNP patients may relate to corticoid resistance.
Source: European Respiratory Journal - November 25, 2021 Category: Respiratory Medicine Authors: Morell, A., Milara, J., Lastovickova, L., Roger, I., Garcia-Lliberos, A., Zapater-Latorre, E., Armengot, M., Cortijo, J., Wsol, V. Tags: Airway pharmacology and treatment Source Type: research
