LncRNA SSTR5-AS1 promotes esophageal carcinoma through regulating ITGB6/JAK1/STAT3 signaling

Zhaohui Tang1, Yongjun Jiang1, Yuyu Zong1

  • 1Department of Oncology, The Central Hospital of Yongzhou, Hunan Province, Yongzhou, 425000, China.

Epigenomics
|September 5, 2024
PubMed

Insights

Somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) promotes esophageal carcinoma (ESCA) growth. Silencing SSTR5-AS1 inhibits ESCA cell invasion and migration by regulating the integrin beta 6 (ITGB6)/JAK1/STAT3 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Esophageal carcinoma (ESCA) is a significant global health concern.
  • The role of non-coding RNAs, such as antisense RNAs, in cancer development is an emerging area of research.

Purpose of the Study:

  • To elucidate the functional role of somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) in the pathogenesis of esophageal carcinoma.
  • To investigate the molecular mechanisms underlying SSTR5-AS1's influence on ESCA cell behavior.

Main Methods:

  • Cellular function assays including EdU staining and Transwell assays were employed.
  • Fluorescence in situ hybridization (FISH) was used to determine the subcellular localization of SSTR5-AS1.
  • RNA interference (shRNA) was utilized to silence SSTR5-AS1 expression in ESCA cells.

Main Results:

  • SSTR5-AS1 shRNA significantly repressed invasion and migration while inducing apoptosis in ESCA cells.
  • SSTR5-AS1 was found to be localized in the cytoplasm and regulates integrin beta 6 (ITGB6) expression via eukaryotic translation initiation factor 4A3 (EIF4A3).
  • Silencing SSTR5-AS1 inactivated the ITGB6 and JAK1/STAT3 signaling pathways, attenuating malignant behaviors in ESCA cells.

Conclusions:

  • SSTR5-AS1 promotes ESCA tumorigenesis by interacting with EIF4A3 to modulate the ITGB6/JAK1/STAT3 axis.
  • SSTR5-AS1 represents a potential therapeutic target for esophageal carcinoma.
  • Understanding the SSTR5-AS1 regulatory network provides a basis for developing novel anti-ESCA strategies.

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