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Published Erratum
. 2025 Jun 10:16:443-444.
doi: 10.18632/oncotarget.28746.

Correction: Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b

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Published Erratum

Correction: Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b

Elisabetta Vergani et al. Oncotarget. .
No abstract available

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Figures

Figure 5
Figure 5. Concerted HIF1A and CCL2 regulation.
(A) HIF1A gene expression analysis showing upregulation in LM16-R cells compared to LM16-S cells, reduction upon CCL2 silencing (siCCL2), and an increase in LM16-S cells treated with rCCL2 at 100 ng/mL for 24 h. Actin was used as the internal reference and LM16-S or siControl as the calibrator. Relative quantification (RQ) values obtained by qRT-PCR are shown. *** p < 0.0001 and * p < 0.05 by unpaired t-test. (B) Increase in HIF1A gene expression in melanoma cell lines upon PLX4032 treatment. 2−ΔCt values are shown. * p < 0.05 by Mann-Whitney U-test. (C) Analysis of the correlation between the CCL2 and HIF1A gene expression levels in melanoma tissues from patients (n = 20). The rs and p-values resulting from Spearman analysis are shown. (D) Expression levels of HIF1 targets in LM16-R compared to LM16-S cell lines. FACS analysis detection of EGFR, integrin α1 and integrin α5. Percentages of protein expression are shown in the graph. (E) Expression of COX2 in LM16-S and LM16-R cells as detected by western blot analysis; production of MMP-2/-9 as detected by gelatin zymography in supernatants from LM16-S and LM16-R cells.

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