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It has been widely accepted that long-noncoding RNA (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) emerges as a crucial mediator in inflammation. Here, we first detected HOTAIR in lipopolysaccharide (LPS)-treated normal human liver cell line (L02) and hepatocellular carcinoma cell lines (C3A, HepG2, and SMMC-7721). Further, we explored the biological function of HOTAIR in LPS-induced hepatocytes (L02 and C3A) lesions and investigated the molecular mechanisms. Besides, we focused on inflammatory signaling crosstalk. The inflammatory insults were assayed by cell counting kit-8 (CCK-8), cell cycle and apoptosis analysis kit, and immunoblotting assay. HOTAIR level was examined by reverse-transcription polymerase chain reaction. To determine the effect of HOTAIR silence or overexpression in inflammation, we applied quantitative reverse-transcription polymerase chain reaction, immunoblotting assay, and enzyme-linked immuno sorbent assay. Regulator inhibitors of Janus kinase/signal transducer and activator of transcription (JAK2/STAT3; AG490) and nuclear factor κB (NF-κB; BAY-11-7082) were applied to treat cells. Our results suggested that LPS induced the overexpression of HOTAIR in L02, C3A, HepG2, and SMMC-7721 cells. LPS repressed viability, induced apoptosis, and facilitated the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in L02 and C3A cells. IL-1β, IL-6, and TNF-α were upregulated by HOTAIR overexpression while downregulated by HOTAIR knockdown in LPS-treated cells. We further observed that HOTAIR overexpression accelerated LPS-induced phosphorylation whereas HOTAIR silence blocked this progress. Inhibition of JAK/STAT and NF-κB contributed to the suppression of cytokines which was evoked by LPS. Collectively, our findings indicated that HOTAIR exerted a crucial role in cytokines expression by activating JAK/STAT and NF-κB.

Titel:	HOTAIR regulates lipopolysaccharide-induced inflammatory response in hepatocytes.
Autor/in / Beteiligte Person:	Zhang, J ; Chen, M ; Zhai, Y ; Fu, Y
Link:	Full Text Finder (Volltext)
Zeitschrift:	Journal of cellular physiology, Jg. 235 (2020-05-01), Heft 5, S. 4247-4255
Veröffentlichung:	New York, NY : Wiley-Liss ; <i>Original Publication</i>: Philadelphia, Wistar Institute of Anatomy and Biology., 2020
Medientyp:	academicJournal
ISSN:	1097-4652 (electronic)
DOI:	10.1002/jcp.29301
Schlagwort:	Apoptosis Cell Line Cell Survival Cytokines genetics Cytokines metabolism Gene Expression Regulation drug effects Gene Expression Regulation physiology Hepatocytes metabolism Humans Janus Kinases genetics Janus Kinases metabolism NF-kappa B genetics NF-kappa B metabolism Nitriles pharmacology RNA, Long Noncoding genetics STAT Transcription Factors genetics STAT Transcription Factors metabolism Sulfones pharmacology Hepatocytes drug effects Inflammation chemically induced Inflammation metabolism Lipopolysaccharides toxicity RNA, Long Noncoding metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Retracted Publication Language: English [J Cell Physiol] 2020 May; Vol. 235 (5), pp. 4247-4255. <i>Date of Electronic Publication: </i>2019 Oct 17. MeSH Terms: Hepatocytes / drug effects ; Inflammation / chemically induced ; Inflammation / metabolism ; Lipopolysaccharides / toxicity ; RNA, Long Noncoding / *metabolism ; Apoptosis ; Cell Line ; Cell Survival ; Cytokines / genetics ; Cytokines / metabolism ; Gene Expression Regulation / drug effects ; Gene Expression Regulation / physiology ; Hepatocytes / metabolism ; Humans ; Janus Kinases / genetics ; Janus Kinases / metabolism ; NF-kappa B / genetics ; NF-kappa B / metabolism ; Nitriles / pharmacology ; RNA, Long Noncoding / genetics ; STAT Transcription Factors / genetics ; STAT Transcription Factors / metabolism ; Sulfones / pharmacology Comments: Retraction in: J Cell Physiol. 2022 Feb;237(2):1618. (PMID: 34087006) References: Banerjee, S., Biehl, A., Gadina, M., Hasni, S., & Schwartz, D. M. (2017). JAK-STAT signaling as a target for inflammatory and autoimmune diseases: Current and future prospects. Drugs, 77(5), 521-546. ; Duan, G., Song, S., & Niu, S. (2018). WITHDRAWN: Long non-coding RNA HOTAIR promotes LPS-induced inflammatory injury by down-regulation of microRNA-124 in murine chondrogenic ATDC5 cells. Life Sciences, S0024-S3205. ; Endig, J., Buitrago-Molina, L. E., Marhenke, S., Reisinger, F., Saborowski, A., Schütt, J., … Vogel, A. (2016). Dual role of the adaptive immune system in liver injury and hepatocellular carcinoma development. Cancer Cell, 30(2), 308-323. ; Fujisaka, Y., Iwata, T., Tamai, K., Nakamura, M., Mochizuki, M., Shibuya, R., … Satoh, K. (2018). Long non-coding RNA HOTAIR up-regulates chemokine (C-C motif) ligand 2 and promotes proliferation of macrophages and myeloid-derived suppressor cells in hepatocellular carcinoma cell lines. Oncology Letters, 15(1), 509-514. ; Geng, Y., Xie, S., Li, Q., Ma, J., & Wang, G. (2011). Large intervening non-coding RNA HOTAIR is associated with hepatocellular carcinoma progression. Journal of International Medical Research, 39(6), 2119-2128. ; Grivennikov, S., Karin, E., Terzic, J., Mucida, D., Yu, G. Y., Vallabhapurapu, S., … Karin, M. (2009). IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer. Cancer Cell, 15(2), 103-113. ; Große, L., Wurm, C. A., Brüser, C., Neumann, D., Jans, D. C., & Jakobs, S. (2016). Bax assembles into large ring-like structures remodeling the mitochondrial outer membrane in apoptosis. The EMBO Journal, 35(4), 402-413. ; Gupta, R. A., Shah, N., Wang, K. C., Kim, J., Horlings, H. M., Wong, D. J., … Chang, H. Y. (2010). Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Nature, 464(7291), 1071-1076. ; Hajjar, A. M., Ernst, R. K., Tsai, J. H., Wilson, C. B., & Miller, S. I. (2002). Human Toll-like receptor 4 recognizes host-specific LPS modifications. Nature Immunology, 3(4), 354-359. ; He, G., & Karin, M. (2011). NF-κB and STAT3 - key players in liver inflammation and cancer. Cell Research, 21(1), 159-168. ; Ishibashi, M., Kogo, R., Shibata, K., Sawada, G., Takahashi, Y., Kurashige, J., … Mori, M. (2013). Clinical significance of the expression of long non-coding RNA HOTAIR in primary hepatocellular carcinoma. Oncology Reports, 29(3), 946-950. ; Jayaraman, P., Sada-Ovalle, I., Nishimura, T., Anderson, A. C., Kuchroo, V. K., Remold, H. G., & Behar, S. M. (2013). IL-1β promotes antimicrobial immunity in macrophages by regulating TNFR signaling and caspase-3 activation. The Journal of Immunology, 190(8), 4196-4204. ; Johnson, C., Han, Y., Hughart, N., McCarra, J., Alpini, G., & Meng, F. (2012). Interleukin-6 and its receptor, key players in hepatobiliary inflammation and cancer. Translational Gastrointestinal Cancer, 1(1), 58-70. ; Kim, H. J., Lee, D. W., Yim, G. W., Nam, E. J., Kim, S., Kim, S. W., & Kim, Y. T. (2015). Long non-coding RNA HOTAIR is associated with human cervical cancer progression. International Journal of Oncology, 46(2), 521-530. ; Li, K., Li, N. L., Wei, D., Pfeffer, S. R., Fan, M., & Pfeffer, L. M. (2012). Activation of chemokine and inflammatory cytokine response in hepatitis C virus-infected hepatocytes depends on Toll-like receptor 3 sensing of hepatitis C virus double-stranded RNA intermediates. Hepatology, 55(3), 666-675. ; Li, Z. Q., Gu, X. Y., Hu, J. X., Ping, Y., Li, H., Yan, J. Y., … Zhang, Y. (2016). Hepatitis C virus core protein impairs metabolic disorder of liver cell via HOTAIR-Sirt1 signalling. Bioscience Reports, 36(3), e00336. ; Luedde, T., & Schwabe, R. F. (2011). NF-κB in the liver--linking injury, fibrosis and hepatocellular carcinoma. Nature Reviews Gastroenterology & Hepatology, 8(2), 108-118. ; Obaid, M., Udden, S. M. N., Deb, P., Shihabeddin, N., Zaki, M. H., & Mandal, S. S. (2018). LncRNA HOTAIR regulates lipopolysaccharide-induced cytokine expression and inflammatory response in macrophages. Scientific Reports, 8(1), 15670. ; Odena, G., Chen, J., Lozano, J. J., Altamirano, J., Rodrigo-Torres, D., Affo, S., … Bataller, R. (2016). LPS-TLR4 pathway mediates ductular cell expansion in alcoholic hepatitis. Scientific Reports, 6, 35610. ; Pang, J. L., Wang, J. W., Hu, P. Y., Jiang, J. S., & Yu, C. (2018). HOTAIR alleviates ox-LDL-induced inflammatory response in Raw264.7 cells via inhibiting NF-κB pathway. European Review for Medical and Pharmacological Sciences, 22(20), 6991-6998. ; Park, J., Kang, W., Ryu, S. W., Kim, W. I., Chang, D. Y., Lee, D. H., … Choi, C. (2012). Hepatitis C virus infection enhances TNFalpha-induced cell death via suppression of NF-kappaB. Hepatology (Baltimore, Md), 56(3), 831-840. ; Park, K. S., Choi, K. H., Kim, Y. S., Hong, B. S., Kim, O. Y., Kim, J. H., … Gho, Y. S. (2010). Outer membrane vesicles derived from Escherichia coli induce systemic inflammatory response syndrome. PLOS One, 5(6), e11334. ; Ringelhan, M., Pfister, D., O'Connor, T., Pikarsky, E., & Heikenwalder, M. (2018). The immunology of hepatocellular carcinoma. Nature Immunology, 19(3), 222-232. ; Robinson, M. W., Harmon, C., & O'Farrelly, C. (2016). Liver immunology and its role in inflammation and homeostasis. Cellular & Molecular Immunology, 13(3), 267-276. ; Samavati, L., Rastogi, R., Du, W., Hüttemann, M., Fite, A., & Franchi, L. (2009). STAT3 tyrosine phosphorylation is critical for interleukin 1 beta and interleukin-6 production in response to lipopolysaccharide and live bacteria. Molecular Immunology, 46(8-9), 1867-1877. ; Schindler, C., Levy, D. E., & Decker, T. (2007). JAK-STAT signaling: From interferons to cytokines. Journal of Biological Chemistry, 282(28), 20059-20063. ; Siddiqui, W. A., Ahad, A., & Ahsan, H. (2015). The mystery of BCL2 family: Bcl-2 proteins and apoptosis: An update. Archives of Toxicology, 89(3), 289-317. ; Siegel, R. L., Miller, K. D., & Jemal, A. (2018). Cancer statistics, 2018. CA: A Cancer Journal for Clinicians, 68(1), 7-30. ; Soares, J. B., Pimentel-Nunes, P., Afonso, L., Rolanda, C., Lopes, P., Roncon-Albuquerque, R., Jr., … Leite-Moreira, A. F. (2012). Increased hepatic expression of TLR2 and TLR4 in the hepatic inflammation-fibrosis-carcinoma sequence. Innate Immunity, 18(5), 700-708. ; Subramaniam, A., Shanmugam, M. K., Perumal, E., Li, F., Nachiyappan, A., Dai, X., … Sethi, G. (2013). Potential role of signal transducer and activator of transcription (STAT)3 signaling pathway in inflammation, survival, proliferation and invasion of hepatocellular carcinoma. Biochimica et Biophysica Acta, 1835(1), 46-60. ; Svinka, J., Mikulits, W., & Eferl, R. (2014). STAT3 in hepatocellular carcinoma: New perspectives. Hepatic Oncology, 1(1), 107-120. ; Wan, Y., Freeswick, P. D., Khemlani, L. S., Kispert, P. H., Wang, S. C., Su, G. L., & Billiar, T. R. (1995). Role of lipopolysaccharide (LPS), interleukin-1, interleukin-6, tumor necrosis factor, and dexamethasone in regulation of LPS-binding protein expression in normal hepatocytes and hepatocytes from LPS-treated rats. Infection and Immunity, 63(7), 2435-2442. ; Wu, H., Liu, J., Li, W., Liu, G., & Li, Z. (2016). LncRNA-HOTAIR promotes TNF-α production in cardiomyocytes of LPS-induced sepsis mice by activating NF-κB pathway. Biochemical and Biophysical Research Communications, 471(1), 240-246. ; Yang, J., Liao, X., Agarwal, M. K., Barnes, L., Auron, P. E., & Stark, G. R. (2007). Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFkappaB. Genes & Development, 21(11), 1396-1408. ; Yoshigai, E., Hara, T., Inaba, H., Hashimoto, I., Tanaka, Y., Kaibori, M., … Nishizawa, M. (2014). Interleukin-1beta induces tumor necrosis factor-alpha secretion from rat hepatocytes. Hepatology Research, 44(5), 571-583. ; Yu, H., Pardoll, D., & Jove, R. (2009). STATs in cancer inflammation and immunity: A leading role for STAT3. Nature Reviews Cancer, 9(11), 798-809. ; Zhang, C., Wang, P., Jiang, P., Lv, Y., Dong, C., Dai, X., … Wang, Z. (2016). Upregulation of lncRNA HOTAIR contributes to IL-1β-induced MMP overexpression and chondrocytes apoptosis in temporomandibular joint osteoarthritis. Gene, 586(2), 248-253. ; Zhang, E., & Lu, M. (2015). Toll-like receptor (TLR)-mediated innate immune responses in the control of hepatitis B virus (HBV) infection. Medical Microbiology and Immunology, 204(1), 11-20. ; Özeş, A. R., Miller, D. F., Özeş, O. N., Fang, F., Liu, Y., Matei, D., … Nephew, K. P. (2016). NF-κB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer. Oncogene, 35(41), 5350-5361. Contributed Indexing: Keywords: HOTAIR; JAK/STAT; NF-ΚB; cytokines; inflammation Substance Nomenclature: 0 (3-(4-methylphenylsulfonyl)-2-propenenitrile) ; 0 (Cytokines) ; 0 (HOTAIR long untranslated RNA, human) ; 0 (Lipopolysaccharides) ; 0 (NF-kappa B) ; 0 (Nitriles) ; 0 (RNA, Long Noncoding) ; 0 (STAT Transcription Factors) ; 0 (Sulfones) ; EC 2.7.10.2 (Janus Kinases) Entry Date(s): Date Created: 20191018 Date Completed: 20210309 Latest Revision: 20210604 Update Code: 20231215

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HOTAIR regulates lipopolysaccharide-induced inflammatory response in hepatocytes.