TMEM161B‐AS1 suppresses proliferation, invasion and glycolysis by targeting miR‐23a‐3p/HIF1AN signal axis in oesophageal squamous cell carcinoma

Mounting data have shown that long non‐coding RNAs (lncRNAs) widely participate in tumour initiation, development, progression and glycolysis in a variety of tumours. However, the clinical prognosis and molecular mechanisms of TMEM161B‐AS1 in oesophageal squamous cell carcinoma (ESCC) remain still unknown. Here, TMEM161B‐AS1 and HIF1AN were significantly lower in ESCC tissues than in normal samples, and their low expressions were both related to TNM stage, lymph node metastasis and poor prognosis of ESCC patients. Functionally, TMEM161B‐AS1 overexpression or miR‐23a‐3p depletion suppressed the proliferation, invasion and glycolysis as well as reduced glucose consumption and lactate production in ESCC cells. Mechanistically, TMEM161B‐AS1 manipulated HIF1AN expression by competitively sponging miR‐23a‐3p in ESCC cells. MiR‐23a‐3p mimic and HIF1AN siRNA partly reversed cell phenotypes mediated by TMEM161B‐AS1 in ESCC cells. Collectively, TMEM161B‐AS1, miR‐23a‐3p and HIF1AN may be tightly involved in ESCC development and progression as well as patients’ prognosis, and TMEM161B‐AS1/miR‐23a‐3p/HIF1AN signal axis may be a promising target for the treatment of ESCC patients.