Research Paper Volume 13, Issue 10 pp 14198—14218

LncRNA LOC146880 promotes esophageal squamous cell carcinoma progression via miR-328-5p/FSCN1/MAPK axis

FSCN1 regulates ESCC cell growth and progression via MAPK signaling pathway in a LOC146880-dependent manner. (A–D) Western blotting analysis shows levels of FSCN1 and MAPK signaling pathway proteins, MEK (1/2), ERK (1/2), p-MEK (1/2) and p-ERK (1/2) in (A) Kyse30, TE-1 transfected with control and si-FSCN1, (B) Kyse30 and TE-1 cells transfected with miR-NC, miR-328-5p mimics and miR-328-5p inhibitors, and (C) control and LOC146880-silenced ESCC cells, (D) Kyse30 and TE-1 cells transfected with scrambled, si-LOC146880#2, miR-328-5p inhibitors, miR-328-5p inhibitors plus si-LOC146880#. (E) Schematic representation shows that H3K27 acetylation-induced LOC146880 over-expression promotes ESCC growth and progression by upregulating FSCN1/MAPK signaling pathway via sponging of miR-328-5p.

Figure 6. FSCN1 regulates ESCC cell growth and progression via MAPK signaling pathway in a LOC146880-dependent manner. (AD) Western blotting analysis shows levels of FSCN1 and MAPK signaling pathway proteins, MEK (1/2), ERK (1/2), p-MEK (1/2) and p-ERK (1/2) in (A) Kyse30, TE-1 transfected with control and si-FSCN1, (B) Kyse30 and TE-1 cells transfected with miR-NC, miR-328-5p mimics and miR-328-5p inhibitors, and (C) control and LOC146880-silenced ESCC cells, (D) Kyse30 and TE-1 cells transfected with scrambled, si-LOC146880#2, miR-328-5p inhibitors, miR-328-5p inhibitors plus si-LOC146880#. (E) Schematic representation shows that H3K27 acetylation-induced LOC146880 over-expression promotes ESCC growth and progression by upregulating FSCN1/MAPK signaling pathway via sponging of miR-328-5p.