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. Author manuscript; available in PMC: 2023 Nov 1.
Published in final edited form as: Mol Cancer Res. 2023 May 1;21(5):397–410. doi: 10.1158/1541-7786.MCR-21-0832

Figure 2. Vemurafenib-resistant BRAFV600E thyroid cancer clones exhibit higher p-ERK level upon vemurafenib treatment.

Figure 2.

(A) Schematics of generation of clonally-selected Vem-resistant 8505C and WRO clones. (B) Representative western blot images show the level of p-ERK, t-ERK, and GAPDH in resistant 8505C and WRO clones relative to parental cells after Vem treatment (2μM, 72hr). Each band intensity in immunoblots were quantified using ImageJ software. p-ERK to t-ERK levels were normalized to the GAPDH expression in each experimental condition (The normalized p-ERK level in untreated, parental cells is set to 1). The experiment was repeated at least three times. (C) MTT analysis shows that 8505C-Res-1 clone is more resistant to Vem than parental 8505C. (n = 9 per group). (D) Representative western blot images of Vem-resistant Res-1 clone vs. parental 8505C upon Vem treatment (0.5 or 2 μM; 24 or 72 hr). (E) Cell viability was assessed by MTT in Vem-resistant Res-6 clone and parental WRO cells after different concentrations of Vem treatment. (F) Representative western blot images of Vem-resistant Res-6 clone vs. parental WRO upon Vem treatment (0.5 or 2 μM; 24 or 72 hr).