Silencing LINC01234 represses pancreatic cancer progression by inhibiting the malignant phenotypes of pancreatic cancer cells |
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| Affiliation: | 1. Second Department of General Surgery, Shanxi Provincial Cancer Hospital, TaiYuan 030013, Shanxi, China;2. Department of Endocrinology, Shanxi Bethune Hospital, TaiYuan 030032, Shanxi, China;1. Department of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara 390002, Gujarat, India;2. C. G. Bhakta Institute of Biotechnology, Uka Tarsadia University, Tarsadi, Surat 394350, Gujarat, India;1. School of Laboratory Medicine and Biotechnology, Southern Medical University, 510515 Guangzhou City, Guangdong Province, China;2. General Hospital of Central Theatre Command, 430070 Wuhan City, Hubei Province, China;1. Servicio de Neumología, Hospital General de México “Dr. Eduardo Liceaga”, Secretaría de Salud, Mexico City, Mexico;2. Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico;3. Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico;4. Departamento de Microbiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico;5. Unidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional “Siglo XXI”, Instituto Mexicano del Seguro Social (IMSS), Mexico City, Mexico;6. Departamento de Genética, Hospital Infantil de México Federico Gómez, Mexico City, Mexico;7. Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA;8. Texas Children''s Hospital, Center for Human Immunobiology, Department of Allergy, Immunology and Rheumatology, Houston, TX, USA;9. Unidad de Desarrollo e Investigación en Bioterapéuticos (UDIBI), Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional. Mexico City, Mexico;10. Laboratorio Nacional para Servicios Especializados de Investigación, Desarrollo e Innovación (l+D+i) para Farmoquímicos y Biotecnológicos, LANSEIDI-FarBiotec-CONACyT. Mexico City, Mexico;11. Coordinación de Investigaciones Inmunológicas, Instituto de Diagnóstico y Referencia Epidemiológicos (InDRE), Secretaria de Salud, Mexico City, Mexico;12. Facultad de Medicina. Universidad Westhill, Mexico City, Mexico;13. Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico;1. Centro Universitário São Camilo, Centro Universitário São Camilo, Av. Nazaré, 1501, São Paulo, Brazil;2. Programa de Pós-graduação Biologia-Química, Instituto de Ciências Ambientais, Químicas e Farmacêuticas, Universidade Federal de São Paulo campus Diadema, Rua São Nicolau, 210, Diadema, Brazil;3. Departamento de Ciências Farmacêuticas, Instituto de Ciências Ambientais, Químicas e Farmacêuticas, Universidade Federal de São Paulo campus Diadema;4. Instituto de Ciências da Saúde, Pós-graduação em Patologia Ambiental e Experimental, Universidade Paulista, Rua Bacelar, 902, São Paulo, Brazil;5. Pós Graduação Interdisciplinar em Saúde, Universidade Cruzeiro do Sul, Rua Galvão Bueno, 868, São Paulo, Brazil;6. Laboratório de Fisiopatologia, Instituto Butantan, Av. Vital Brasil, 1500, São Paulo, Brazil;1. Department of Pediatrics, PKU Care Zibo Hospital, Zibo, Shandong 255069, China;2. Department of Traditional Chinese Medicine, PKU Care Zibo Hospital, Zibo, Shandong 255069, China;3. Department of Ultrasonography, The Zibo 6th Remin Hospital, Zibo, Shandong 255000, China;1. Faculty of Health & Life Sciences, De Montfort University, UK;2. Department of Respiratory Sciences, University of Leicester, UK;3. Warwick Medical School, University of Warwick, UK;4. Biosciences, Brunel University London, Uxbridge, UK;5. Department of Veterinary Medicine, U.A.E. University, Al Ain, United Arab Emirates |
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| Abstract: | ObjectivePrevious works have outlined the pivotal involvement of long intergenic non-coding RNA (lincRNA) in cancer progression, while the efficiency of LINC01234 in pancreatic cancer remained obscure. The purpose of this research is to unravel the regulatory mechanism of LINC01234 in pancreatic cancer via modulating microRNA (miR)-513a-3p and hexose 6-phosphate dehydrogenase (H6PD).MethodsPancreatic cancer cells were cultured and clinical tissue specimens were collected. LINC01234, miR-513a-3p and H6PD levels in pancreatic cancer cells and tissues were examined. Plasmids altering LINC01234, miR-513a-3p and H6PD expression were transfected into pancreatic cancer cells to assess the change in biological behaviors of pancreatic cancer cells. The targeting relations among LINC01234, miR-513a-3p and H6PD were validated.ResultsLINC01234 and H6PD levels were elevated while miR-513a-3p level was reduced in pancreatic cancer cells and tissues. LINC01234 deficiency hindered the malignant biological activities of pancreatic cancer cells. MiR-513a-3p depletion or H6PD elevation could abrogate the inhibitory effects of LINC01234 silencing on pancreatic cancer cells. LINC01234 sponged miR-513a-3p that targeted H6PD.ConclusionThe reduced LINC01234 exerts inhibitory impacts on pancreatic cancer cells via targeting miR-513a-3p to restrain H6PD level. The current study broadens the understanding of LINC01234 function and affords novel therapeutic targets for pancreatic cancer treatment. |
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| Keywords: | Pancreatic cancer Long intergenic non-coding RNA 01,234 MicroRNA-513a-3p Hexose 6-phosphate dehydrogenase Proliferation Apoptosis |
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