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Updated: Jun 14, 2025

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
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.
Abstract:
Aim: To investigate function of somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) in esophageal carcinoma (ESCA).Materials & methods: The cellular function was assessed using EdU staining and Transwell assay. The localization of SSTR5-AS1 was measured using fluorescence in situ hybridization staining.Results: SSTR5-AS1 shRNA repressed invasion and migration and induced apoptosis in ESCA cells. SSTR5-AS1 was distributed in cytoplasm, and it regulated its subunit integrin beta 6 (ITGB6) via eukaryotic translation initiation factor 4A3 (EIF4A3). SSTR5-AS1 shRNA inactivated ITGB6 and JAK1/STAT3 signaling. SSTR5-AS1 silencing attenuated the malignant behavior of ESCA cells through the ITGB6-mediated JAK1/STAT3 axis.Conclusion: SSTR5-AS1 promotes tumorigenesis of ESCA by interacting with EIF4A3 to regulate ITGB6/JAK1/STAT3 axis, which serves a basis for discovering strategies against ESCA.
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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