ArticleMolecular medicine reports2021
Long non‑coding RNA HHIP‑AS1 inhibits lung cancer epithelial‑mesenchymal transition and stemness by regulating PCDHGA9.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 8 citations in OpenAlex.
- Comprehensive landscape and future perspective of long noncoding RNAs in non-small cell lung cancer: it takes a village.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the effect of hedgehog‑interacting protein antisense RNA 1 (HHIP‑AS1) on epithelial‑mesenchymal transition (EMT) and cellular stemness of human lung cancer cells by regulating the microRNA (miR)‑153‑3p/PCDHGA9 axis. Reverse transcription‑quantitative PCR was used to compare the expression of HHIP‑AS1 in lung cancer and adjacent normal lung tissues. In addition, the correlation of HHIP‑AS1 with E‑cadherin, Vimentin, N‑cadherin and Twist1 was analyzed. HHIP‑AS1 overexpression vector was transfected into lung cancer A549 and NCI‑H1299 cell lines. Cell Counting Kit‑8 and Transwell and clonogenic assays were used to detect the proliferation, invasion and clonogenesis of the lung cancer cells, respectively. The associations among HHIP‑AS1, miR‑153‑3p and PCDHGA9 were predicted by bioinformatics analysis and verified by a dual‑luciferase reporter system. The results showed that the expression of HHIP‑AS1 in lung cancer tissues was significantly lower than that in normal tissues (P<0.001). HHIP‑AS1 was positively correlated with E‑cadherin and negatively correlated with Vimentin, N‑cadherin and Twist1. HHIP‑AS1 overexpression inhibited the proliferation, invasion and clonal formation of the A549 and NCI‑H1299 cells. The luciferase reporter system verified that HHIP‑AS1 could adsorb miR‑153‑3p and that PCDHGA9 was the target gene of miR‑153‑3p. A549 cells were transfected with HHIP‑AS1 overexpression vector and miR‑153‑3p mimic, and the miR‑153‑3p mimic had a mitigating effect on HHIP‑AS1 inhibition (P<0.001). In conclusion, HHIP‑AS1 inhibits the EMT and stemness of lung cancer cells by regulating the miR‑153‑3p/PCDHGA9 axis. Thus, HHIP‑AS1 may be a new potential target for lung cancer treatment.
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