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. 2019 May 3;33(3):793–800. doi: 10.21873/invivo.11541

Figure 4. A: Blocking expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) did not alter mammalian target of rapamycin (mTOR) activation by C-C motif chemokine ligand 21 (CCL21). CCL21 at 10 ng/ml was used to treat MyLa cells for 0, 10, 20, 40, and 60 min. Protein lysates were obtained for western blot of mTOR, phospho-(p)-mTOR, extracellular-regulated protein kinases (ERK), p-ERK, signal transducer and activator of transcription 3 (STAT3), pSTAT and actin. A representative blot is shown from two independent experiments. B: mTOR inhibition disrupted CCL21-mediated MALAT1 expression. MyLa cells were pretreated with or without mTOR inhibitor rapamycin for 2 h. The expression of MALAT1 was then measured by real time polymerase chain reaction at 0, 20, 40, and 60 min after CCL21 treatment. Data are presented as means±SD from three independent experiments with triplicates.

Figure 4