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Fig. 5 | Molecular Cancer

Fig. 5

From: LINC01852 inhibits the tumorigenesis and chemoresistance in colorectal cancer by suppressing SRSF5-mediated alternative splicing of PKM

Fig. 5

LINC01852 inhibits aerobic glycolysis through SRSF5-dependent alternative splicing of PKM. (A-D) PKM splicing assays were performed to measure the relative mRNA levels of PKM1 and PKM2 in CRC cells transfected with LINC01852 overexpression plasmid (A), LINC01852-ASOs (B), SRSF5 overexpression plasmid (C) or SRSF5 siRNAs (D). (E) WB was performed to examine the effects of LINC01852 and SRSF5 on the protein levels of PKM1 and PKM2 in CRC cells. (F) RIP assays indicated that SRSF5 directly binds to the flanking region of PKM E10. (G) RNA pull-down assays revealed that SRSF5 strongly binds to a region in PKM E10 (120–126 bp), which contains an exon splicing enhancer (ESE) for SRSF5. (H, I) Effects of LINC01852 and SRSF5 on glucose uptake, lactate production (H), and ATP source (I) in CRC cells. (J) The mRNA levels of PKM1 and PKM2 were positively and negatively correlated, respectively, with the LINC01852 level in CRC tissue samples (n = 23)

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Molecular Cancer

ISSN: 1476-4598