Hsi-Feng Tu1,2, Kuo-Wei Chang1,3, Hui-Wen Cheng4, Chung-Ji Liu1,4,5. 1. Institute of Oral Biology, School of Dentistry, National Yang-Ming University, MacKay Memorial Hospital, Taipei, Taiwan. 2. Department of Dentistry, National Yang-Ming University Hospital, Yi-Lan, Taiwan. 3. Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan. 4. Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan. 5. Department of Oral and Maxillofacial Surgery, MacKay Memorial Hospital, Taipei, Taiwan.
Abstract
OBJECTIVES/HYPOTHESIS: Oral squamous cell carcinoma (OSCC) is prevalent worldwide, and survival in OSCC has not improved significantly in the last few decades. MicroRNAs (miRNAs) have an important regulatory role in human cancer, including oral carcinogenesis. MiR-372 and miR-373 perform oncogenic and tumor-suppressive functions of between different human malignancies. This study investigated the miR-372 and miR-373 expression and their clinical implication in OSCC. METHODS: Fifty patients with primary OSCC were included in the study. Primary cancer cells and matched normal oral epithelium were purified by laser capture microdissection. RNA were extracted from these samples. The expression levels of miR-372 and miR-373 in the tissue of OSCC patients were measured by quantitative reverse transcription polymerase chain reaction. The large tumor suppressor kinase 2 (LATS2) protein expression level was measured by Western blotting. RESULTS: Both miR-372 and miR-373 was up-regulated in OSCC tissue relative to control mucosa. Among different clinical variables, over-expression of miR-372 and miR-373 were associated with nodal metastasis, lymphovascular invasion, and poor survival. Multivariate analysis showed that both high miR-372 and miR-373 expression were independent predictors for poor survival in OSCC. MiR-372 regulated LATS2 expression in OSCC cell lines. LATS2 expression levels are inversely correlated miR-372 in OSCC tissues. CONCLUSION: Over-expression of miR-372 and miR-373 indicate worse survival in OSCC. LEVEL OF EVIDENCE: N/A.
OBJECTIVES/HYPOTHESIS: Oral squamous cell carcinoma (OSCC) is prevalent worldwide, and survival in OSCC has not improved significantly in the last few decades. MicroRNAs (miRNAs) have an important regulatory role in humancancer, including oral carcinogenesis. MiR-372 and miR-373 perform oncogenic and tumor-suppressive functions of between different humanmalignancies. This study investigated the miR-372 and miR-373 expression and their clinical implication in OSCC. METHODS: Fifty patients with primary OSCC were included in the study. Primary cancer cells and matched normal oral epithelium were purified by laser capture microdissection. RNA were extracted from these samples. The expression levels of miR-372 and miR-373 in the tissue of OSCC patients were measured by quantitative reverse transcription polymerase chain reaction. The large tumor suppressor kinase 2 (LATS2) protein expression level was measured by Western blotting. RESULTS: Both miR-372 and miR-373 was up-regulated in OSCC tissue relative to control mucosa. Among different clinical variables, over-expression of miR-372 and miR-373 were associated with nodal metastasis, lymphovascular invasion, and poor survival. Multivariate analysis showed that both high miR-372 and miR-373 expression were independent predictors for poor survival in OSCC. MiR-372 regulated LATS2 expression in OSCC cell lines. LATS2 expression levels are inversely correlated miR-372 in OSCC tissues. CONCLUSION: Over-expression of miR-372 and miR-373 indicate worse survival in OSCC. LEVEL OF EVIDENCE: N/A.
Authors: Joaquim Bellmunt; Chensheng Willa Zhou; Stephanie A Mullane; Lillian Werner; Mary-Ellen Taplin; André P Fay; Toni K Choueiri; Anna Orsola; David Y Takeda; William C Hahn; Jaegil Kim; Guru Sonpavde; Michaela Bowden Journal: Br J Cancer Date: 2016-06-23 Impact factor: 7.640
Authors: Joshua Lubov; Mariana Maschietto; Iman Ibrahim; Alex Mlynarek; Michael Hier; Luiz Paulo Kowalski; Moulay A Alaoui-Jamali; Sabrina Daniela da Silva Journal: Oncotarget Date: 2017-07-13