Fig 1: LGALS2 downregulation promotes more robust in vivo tumor growth. (A) Tumors were analyzed in BALB/c nude mice 6 weeks following injection, with representative endpoint images showing tumors from the OE-CTRL, OE-LGALS2, si-CTRL, and si-LGALS2 groups. (B) Tumor volume monitored over time in the indicated mice (mean ± SD; n=25). **, P<0.01. Animals were euthanized at the experimental endpoint, and tumors were excised. (C) Representative images of IHC staining for Ki-67. (D,E) Quantification of Ki-67 and TUNEL staining of tumors in the indicated groups. (F) LGALS2, PI3K, pAKT, and AKT levels detected via western immunoblotting in the indicated groups, with GAPDH as normalization. All experiments were repeated in triplicate; **, P<0.01. IHC, immunohistochemistry; TUNEL, terminal deoxynucleotidyl transferase (TdT) dUTP nick end labeling.
Fig 2: Correlations between the expression of LGALS2 and PTC patient TNM staging. The correlations between LGALS2 levels and patient N stage (A), T stage (B), and clinical stage (C). *, P<0.05; **, P<0.01. PTC, papillary thyroid carcinoma; TNM, tumor node metastasis.
Fig 3: LGALS2 drives PTC cell apoptotic death via the PI3K/AKT pathway. (A,B) Flow cytometry detects the apoptotic rates for TPC-1 and BHT101 cells following OE-CTRL, OE-LGALS2, si-CTRL, or si-LGALS2 vector transfection. Data are means ± SD. (C) PI3K, pAKT, and AKT detected by western immunoblotting in TPC-1 and BHT101 cells in the indicated treatment groups (OE-CTRL, OE-LGALS2, si-CTRL, and si-LGALS2). (D,E) Protein expression levels are quantified via densitometry, with GAPDH for normalization. All experiments were repeated in triplicate; **, P<0.01. PTC, papillary thyroid carcinoma; PI3K/AKT, phosphatidylinositol-3-kinase/protein kinase B.
Fig 4: LGALS2 downregulation is evident in human PTC tumor tissues and cell lines. (A) LGALS2 mRNA levels are compared via qPCR in PTC and control tissues (n=80). (B) LGALS2 protein levels are significantly lower in PTC patient tumors relative to paracancerous tissues in the four indicated paired tissue samples. (C) Quantification of LGALS2 protein expression in PTC patient tumors and paracancerous tissues (n=21). (D) The AUC curve analyses of LGALS2 expression in PTC and control tissues (n=80). All experiments were repeated in triplicate, and data are means ± SD from triplicate samples; ***, P<0.001; ****, P<0.0001. AUC, area under the curve; PTC, papillary thyroid carcinoma; qPCR, quantitative polymerase chain reaction.
Fig 5: Knocking down LGALS2 enhances the ability of PTC cells to proliferate. (A,B) LGALS2 levels are detected in TPC-1 and BHT101 cells following pcDNA4.0 (OE-CTRL), pcDNA4.0-LGALS2 (OE-LGALS2), NC-siRNA, or LGALS2-siRNA transfection via qPCR and western immunoblotting. (C) LGALS2 upregulation inhibits the ability of TPC-1 and BHT101 cells to proliferate, whereas its knockdown has the opposite effect. (D,E) The comparison of proliferation in OE-CTRL, OE-LGALS2, si-CTRL, and si-LGALS2 groups of TPC-1 and BHT101 cells using an EdU uptake assay. Scale bar: 100 µm. Data are means ± SD from triplicate samples; **, P<0.01; ***, P<0.001. PTC, papillary thyroid carcinoma; qPCR, quantitative polymerase chain reaction.
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