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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: A novel miR-365-3p/EHF/keratin 16 axis promotes oral squamous cell carcinoma metastasis, cancer stemness and drug resistance via enhancing β5-integrin/c-met signaling pathway

Fig. 1

KRT16 expression and its clinical significances in OSCC. a Heat map of the 36 most differentially regulated genes from cDNA microarrays of OC-3-IV (left), OC-3 (middle) and OC-3-IV-M cells (right). b QRT-PCR of mRNAs revealed upregulation of KRT16 mRNA in OSCC tissues compared with their matched normal oral tissues (3.21 ± 0.23-fold change; P = 0.0021). The relative amount of KRT16 normalized to small nuclear RNU6B. RNA was calculated using the eq. 2–ΔCt, where ΔCT = (CTKRT16 RNACTRNU6BRNA). c Retrospective analysis of Kaplan-Meier plots for KRT16 expression in association with relapse-free survival of 294 patients. The level of KRT16 protein was determined through IHC. Tissues expressing KRT16 at levels lower than the median were assigned to the low expression group and those above the median level were assigned to the high expression group. d Retrospective analysis of Kaplan–Meier plots for KRT16 expression in association with overall survival of 294 patients. e Top, typical examples of the expression levels of KRT16 protein as determined through IHC staining in a commercial tissue array slide containing 144 normal and OSCC tissues. Bottom, the table shows the correlation between the KRT16 expression level and OSCC stages. For each section, staining was determined as weak (+), moderate (++), or strong (+++). Specimens were grouped as normal, stage I/II, and stage III/IV. P = 0.0024 for normal versus stage I/II, P = 0.0011 for stage I/II versus stage III/IV

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