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Updated: Feb 5, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
LINC00657 played oncogenic roles in esophageal squamous cell carcinoma by targeting miR-615-3p and JunB
Yuchen Sun1, Jizhao Wang2, Shupei Pan1
1Department of Radiation Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Background:
The prognosis of esophageal squamous cell carcinoma (ESCC) is relatively poor due to the absence of efficient treatment. In this manuscript, we have investigated the specific roles and molecular mechanisms of LINC00657 to order to identify novel therapeutic targets for ESCC.
Method:
The LINC00657 expression in ESCC tissues and cell lines were evaluated by quantitative real-time PCR. The expression of LINC00657 in ESCC cells was regulated by lentivirus transfection. Online bioinformatics analysis tools were used to predict the potential targets of LINC00657 and miR-615-3p. TCGA database was used to analyze the prognosis of ESCC patients. Transwell, wound healing assay and MTT were performed to investigate the ESCC cells' biological functions. JunB expression was evaluated by Western blot.
Result:
LINC00657 was moderately increased in ESCC both in vivo and in vitro and up regulated by irradiation. LINC00657 knockdown could inhibit the migration and proliferation of ESCC cells. And downregulation of LINC00657 significantly enhanced the radio-sensitivity. Moreover, LINC00657 could act as a ceRNA to increase the expression of JunB by binding to miR-615-3p. Meanwhile, overexpression of miR-615-3p resulted in anti-tumor effects and led to the down-regulation of JunB. Survival analysis from TCGA indicated that ESCC patients with higher JunB expression had significant poorer prognosis.
Conclusion:
LINC00657 might be involved in regulating ESCC's response to radiation; and it functioned as an oncogene in ESCC by targeting miR-615-3p and JunB, providing novel potential therapeutic targets.
Insights
Long non-coding RNA LINC00657 acts as an oncogene in esophageal squamous cell carcinoma (ESCC) by targeting miR-615-3p and JunB. Downregulating LINC00657 inhibits ESCC cell growth and enhances radiosensitivity, offering new therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Esophageal squamous cell carcinoma (ESCC) has a poor prognosis due to limited effective treatments.
- Identifying novel therapeutic targets is crucial for improving ESCC patient outcomes.
Purpose of the Study:
- To investigate the role and molecular mechanisms of LINC00657 in ESCC.
- To explore LINC00657 as a potential therapeutic target for ESCC.
Main Methods:
- Quantitative real-time PCR and Western blot were used to assess gene expression.
- Lentivirus transfection was employed to manipulate LINC00657 expression.
- Bioinformatics, TCGA database analysis, Transwell, wound healing, and MTT assays were utilized to evaluate molecular targets and cellular functions.
Main Results:
- LINC00657 expression was elevated in ESCC tissues and cell lines, and upregulated by irradiation.
- LINC00657 knockdown inhibited ESCC cell migration and proliferation, enhancing radiosensitivity.
- LINC00657 acted as a competing endogenous RNA (ceRNA) for miR-615-3p, increasing JunB expression, which correlated with poorer ESCC prognosis.
Conclusions:
- LINC00657 functions as an oncogene in ESCC by targeting the miR-615-3p/JunB axis.
- LINC00657 influences ESCC's response to radiation therapy.
- Targeting LINC00657 presents a promising therapeutic strategy for ESCC.
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