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. 2023 May 8;120(20):e2220334120. doi: 10.1073/pnas.2220334120

Fig. 2.

Fig. 2.

Zn medication eliminates established ESCCs in ZD rats. (A) Study design. (B) Body weights, serum Zn, and testis Zn levels. (C) Tumor multiplicity (number of tumors/esophagus, mean ± SD) (two-tailed Welch t test, n = 8 to 20 rats/cohort); large tumor (size >2 mm) and ESCC incidence (%) (two-tailed Fisher’s exact test; n = 8 to 20 rats/cohort). (D) qPCR analysis of esophageal miR-31 and miR-21 in Zn-treated and Zn-untreated rat esophagus (rat snoRNA as normalizer, two-tailed Welch t test. Error bars represent SD; n = 8 rats per group). (E) Zn treatment induces upregulation of tumor suppressor target PDCD4 (miR-21) and STK40/EGLN3 (miR-31). Black arrowheads in H&E-stained section indicate the presence of apoptotic cells in esophageal epithelium; black arrowheads in near serial PDCD4-stained sections showing abundant/intense nuclear overexpression of PDCD4 in Zn-treated esophagus, compared with sporadic occurrence of apoptotic cells (H&E section) and PDCD4 nuclear expression in isolated/sporadic cells of a Zn-untreated rat (white arrowheads). Representative photos of Zn-treated (n = 21) vs. Zn-untreated (n = 10) esophagus showing H&E staining, IHC staining for STK40, & EGLN3 (brown, 3,3′-diaminobenzidine tetrahydrochloride, DAB) and PDCD4, & PCNA (red, 3-amino-9-ethylcarbazole substrate-chromogen, AEC).