Clinical significance of LINC02532 in hepatitis B virus-associated hepatocellular carcinoma and its regulatory effect on tumor progression - 29/06/24
, Jianguo Wang b, ⁎ Highlights |
• | LINC02532 was a lncRNA abnormally highly expressed in HBV-HCC. |
• | LINC02532 could distinguish HBV-HCC and predict the prognosis of HBV-HCC. |
• | LINC02532 could regulate miR-455–3p. |
• | LINC02532 promoted the malignant characterization of HBV-HCC cells. |
Abstract |
Background and aim |
Long non-coding RNAs (lncRNAs) play an important role in tumor progression, including in hepatocellular carcinoma (HCC) induced by hepatitis B virus (HBV). Therefore, the aim of this study was to investigate the role of LINC02532 in HCC, mainly for diagnostic prognostic value and cellular function, as well as mechanistic aspects.
Methods |
Initially, GEO and VirBase databases were used to screen for aberrant lncRNAs in HBV-HCC.Then, HBV-HCC persons followed up in our center were retrospectively studied to investigate the diagnostic, prognostic value of LINC02532 in HBV-HCC. Subsequently, the role of LINC02532 in HBV-HCC was measured using cellular function assay methods and possible mechanisms were analyzed in conjunction with bioinformatic predictive science.
Results |
LINC02532 was a lncRNA abnormally expressed in HBV-HCC. LINC02532 was significantly up-regulated in the expression level in HBV-HCC tissues compared with normal tissues from patients. Moreover, LINC02532 could distinguish HBV-HCC and predict the prognosis of HBV-HCC. In vitro experiments showed that LINC02532 could regulate miR-455–3p and promote the malignant characterization of HBV-HCC cells. CHEK2 was a target gene of miR-455–3p.
Conclusions |
: The prognosis and diagnosis of HBV-HCC can rely on the expression of LINC02532. LINC02532 was important for further progression of HBV-HCC, by moderating miR-455–3p/CHEK2.
Il testo completo di questo articolo è disponibile in PDF.Keywords : LINC02532, Hepatocellular carcinoma, Hepatitis B infection, Overall survival, Cell function
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Vol 48 - N° 7
Articolo 102403- Agosto 2024 Ritorno al numero
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