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Fig. 2 | Molecular Cancer

Fig. 2

From: Long non-coding RNA NORAD/miR-224-3p/MTDH axis contributes to CDDP resistance of esophageal squamous cell carcinoma by promoting nuclear accumulation of β-catenin

Fig. 2

NORAD contributes to CDDP resistance of ESCC. a The expression of NORAD in CDDP resistant and matched parental ESCC cells, normalized to GAPDH expression. b Representative images of RNA FISH of NORAD in KYSE30/CDDP-R and KYSE30 cells (× 400), which show that NORAD is predominantly located in the cytoplasm. Nuclei are stained with DAPI. c NORAD knockdown increases the sensitivity of KYSE30/CDDP-R cells to CDDP, detected by CCK-8 assay. d Overexpression of NORAD decreases the sensitivity of KYSE30 cells to CDDP, detected by CCK-8 assay. e NORAD knockdown decreases the colony formation ability in KYSE30/CDDP-R cells in the presence of CDDP. f Overexpression of NORAD increases the colony formation ability of KYSE30 in the presence of CDDP. g NORAD knockdown increases the CDDP-induced apoptosis rate in KYSE30/CDDP-R cells, and overexpression of NORAD decreases this rate in KYSE30 cells, detected by FCM. h NORAD knockdown facilitates CDDP to induce cell cycle arrest in KYSE30/CDDP-R cells. i Overexpression of NORAD suppresses CDDP-induced cell cycle arrest in KYSE30 cells. j NORAD knockdown increases the CDDP-induced γH2AX and cleaved caspase-3 in KYSE30/CDDP-R cells. k Overexpression of NORAD decreases the CDDP-induced γH2AX and cleaved caspase-3 in KYSE30 cells. In all cases, error bars denote SD of triplicates. **P < 0.01, ***P < 0.001

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