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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: HMGB1-mediated autophagy regulates sodium/iodide symporter protein degradation in thyroid cancer cells

Fig. 1

HMGB1 expression became up-regulated in thyroid cancer and was associated with clinicopathologic features (a) Western blot of HMGB1 and actin in various cell lines hinted at an over-expression of HMGB1 in thyroid cancer; (b) Immunohistochemical staining of HMGB1 was performed for different tissues. TC, thyroid cancer; TA, thyroid adenoma; SG, simple goiter; N, normal thyroid; PTC, papillary thyroid carcinoma; FTC, follicular thyroid carcinoma; (c) Relative expression levels of HMGB1 in different tissues. Total mRNA was extracted from normal or patient tissues and HMGB1 level determined by relative optical intensity (in arbitrary units, AU) of bands on RT-PCR. Each dot represented relative level of HMGB1 in each individual sample. *P < 0.01 vs. normal thyroid; **P > 0.01 vs. normal thyroid; #P > 0.01 vs. normal thyroid; (d) Relative expression levels of HMGB1 in thyroid cancer. Total mRNA was extracted from thyroid cancer patients’ tissues and HMGB1 level determined by relative optical intensity (in arbitrary units, AU) of bands on RT-PCR. Each dot represented relative level of HMGB1 in an individual sample. *P > 0.01 vs. FTC; (e) HMGB1 expression level for differentiating thyroid cancer tissues from non-thyroid cancer tissues in our validated cohort; AUC: 96.7%, sensitivity: 88.9% and specificity: 96.2% in the validated cohort

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