Background HOMEOBOX A11 (HOXA11) antisense RNA (HOXA11‐AS), a newly identified long noncoding RNAs, is involved in the carcinogenic process of several human tumors. However, the role of HOXA11‐AS in liver cancer progression is not well understood. Materials and Methods This study used liver cancer tissues and cell lines (CSQT‐2 and HCCLM3) to explore the potential mechanism of HOXA11‐AS. Quantitative real‐time polymerase chain reaction and Western blot were applied to evaluate the bio‐molecules expression. Bioinformatics analysis, RNA pull down and luciferase report assay were applied to determine the molecules bind. MTT, transwell, and wound healing assay were used to measure the cell growth situation. Results HOXA11‐AS was highly expressed in liver cancer tissues and cell lines, which was closely related with poor prognosis in patients with liver cancer. HOXA11‐AS could act as a competing endogenous RNA for miR‐15a‐3p. Besides, miR‐15a‐3p negatively controlled its target molecule signal transducer and activator of transcription 3 (STAT3). Furthermore, a linear regression analysis and biological experiments showed a positive correlation between HOAX11‐AS and STAT3. Moreover, HOAX11‐AS overexpression activated the Janus kinase (JAK)‐STAT pathway and thus promoted the growth, migration, and invasion of liver cancer cells, which might be through regulating miR‐15a‐3p/STAT3 axis. Conclusion Our study suggested that HOAX11‐AS could regulate the JAK‐STAT signaling pathway by miR‐15a‐3p/STAT3 axis to promote the progression of liver cancer. Thus, HOXA11‐AS may be regarded as an effective biomarker with diagnostic, prognostic, and therapeutic potentials for liver cancer.

Gastric cancer (GC) is a leading cause of cancer-related death with poor prognosis. Growing evidence has shown that long noncoding ribonucleic acid (lncRNA) FEZ family zinc finger 1 antisense RNA 1(FEZF1-AS1), an “oncogene,” regulates tumor progression and supports cancer stem cell. However, the tumorigenic mechanism of FEZF1-AS1 on gastric cancer stem cell (GCSC) is yet to be investigated. Here, we discovered that FEZF1-AS1 was upregulated in GC tissues and cell lines. Knockdown of FEZF1-AS1 inhibited sphere formation and decreased expression of stem factors and markers. Moreover, FEZF1-AS1 silence also suppressed cell proliferation, viability, invasion, and migration of GCSCs. MiR-363-3p is used as a target of FEZF1-AS1, because its expression was suppressed by FEZF1-AS1 in GCSCs. FEZF1-AS1 could sponge miR-363-3p and increased the expression of high-mobility group AT-hook 2 (HMGA2). The expression of FEZF1-AS1 and miR-363-3p, as well as that of miR-363-3p and HMGA2, was negatively correlated in GC tissues. Finally, FEZF1-AS1 contributed to promotion of GCSCs progression partially through inhibition of miR-363-3p. Subcutaneous xenotransplanted tumor model revealed that silence of FEZF1-AS1 suppressed in vivo tumorigenic ability of GSCS via downregulation of HMGA2. In general, our findings clarified the critical regulatory role of FEZF1-AS1/miR-363-3p/HMGA2 axis in GCSC progression, providing a potential therapeutic target for GC.

No abstract