LncRNA PCBP1-AS1 suppresses cell growth in oral squamous cell carcinoma by targeting miR-34c-5p/ZFP36 axis

Orkideh Shafiee Allaf1, Wenhao Li2, Chongmai Zeng3

  • 1Department of Orthodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, Guangdong, 510055, China. orkideh@163.com.

Insights

Long noncoding RNA PCBP1-AS1 is downregulated in oral squamous cell carcinoma (OSCC). PCBP1-AS1 suppresses OSCC cell growth by upregulating ZFP36 via interaction with miR-34c-5p.

Area of Science:

  • Molecular biology
  • Oncology
  • Genetics

Background:

  • Oral squamous cell carcinoma (OSCC) is a prevalent and dangerous oral malignancy.
  • Bioinformatics analysis indicates long noncoding RNA PCBP1-AS1 is downregulated in OSCC.
  • Understanding the role of PCBP1-AS1 in OSCC is crucial for developing new therapeutic strategies.

Purpose of the Study:

  • To investigate the functions and molecular mechanisms of PCBP1-AS1 in OSCC.
  • To determine the expression levels of PCBP1-AS1 in OSCC cells.
  • To elucidate the regulatory pathway involving PCBP1-AS1, miR-34c-5p, and ZFP36 in OSCC.

Main Methods:

  • Quantitative polymerase chain reaction (qPCR) for gene expression analysis.
  • Cell viability, proliferation (CCK-8, colony-forming assays), and apoptosis (TUNEL, flow cytometry) assays.
  • RNA immunoprecipitation (RIP), RNA pulldown, and luciferase reporter assays to identify molecular interactions.

Main Results:

  • PCBP1-AS1 expression was found to be significantly downregulated in OSCC cells.
  • Overexpression of PCBP1-AS1 inhibited OSCC cell proliferation and induced apoptosis.
  • PCBP1-AS1 directly interacted with miR-34c-5p, negatively regulating its expression.
  • miR-34c-5p targeted the 3'untranslated region of ZFP36.
  • PCBP1-AS1 positively regulated ZFP36 expression, and ZFP36 silencing reversed the effects of PCBP1-AS1.

Conclusions:

  • PCBP1-AS1 acts as a tumor suppressor in OSCC.
  • PCBP1-AS1 inhibits OSCC cell growth by upregulating ZFP36 through the miR-34c-5p pathway.
  • This regulatory axis presents a potential therapeutic target for OSCC treatment.

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