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. Author manuscript; available in PMC: 2021 May 28.
Published in final edited form as: Cancer Lett. 2020 Mar 4;478:8–21. doi: 10.1016/j.canlet.2020.02.040

Figure 6. miR-6778–5p-SHMT1 signalling contributes to GCSC maintenance via regulation of cytoplasmic one-carbon metabolism.

Figure 6.

(A) Histograms show the sphere volumes of GCSCs derived from the indicated gastric cancer cells. Addition of serine (0.8 mM) could party rescue CSC formation in miR-6778–5p or SHMT1-knockdown gastric cancer cells and could especially rescue CSC formation in Drosha-knockdown gastric cancer cells. (B) Isotopic tracing analysis of relative M+1 and M+2 dTTP in GCSCs derived from Drosha WT and Drosha KD MGC-803 cells cultured in medium with [2,3,3-2H]-serine. (C) Isotopic tracing analysis of M+1 and M+2 dTTP in GCSCs derived from the indicated gastric cancer cells cultured in medium with [2,3,3-2H]-serine. (D) Histograms show the sphere volumes of GCSCs derived from the indicated Drosha WT or Drosha KD gastric cancer cells treated with or without 30 μg/ml of 5-FU (a chemotherapeutic drug for gastric cancer). (E) The miR-6778–5p, SHMT1 and CD44 levels in gastric tumour tissues and their control normal tissues and 5-FU sensitive or resistant gastric tumour tissues were evaluated by qRT-PCR.