Related Experiment Video
Updated: Dec 26, 2025
Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
Published on: August 11, 2017
LINC00152 Knock-down Suppresses Esophageal Cancer by EGFR Signaling Pathway
Yan Ding1,2, Hai Guo3, Liangjun Zhu4
1Department of Oncology, BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing 210019, China.
Aim:
This study aims to explain the role and mechanism of lncRNA LINC00152 in esophageal cancer.
Methods:
The 30 pairs of esophageal cancer and adjacent normal tissues were collected and measuring the lncRNA LINC00152 expression by ISH and RT-qPCR assay. In the next cell experiment, Eca 109 and Kyse 150 cells were divided into 3 groups: NC group were treated with non-treatment; BL group were transfected with empty vector and lncRNA group were transfected with lncRNA LINC00152. The cells proliferation were measured by MTT assay; the cells apoptosis and cell cycle were evaluated by flow cytometry. The relative proteins expressions were measured by WB assay.
Results:
Compared with NC groups, the cell proliferation rate of lncRNA groups were significantly suppressed (P<0.05, respectively); the cell apoptosis and G1 phase rates were significantly enhanced in the lncRNA groups (P<0.05, respectively). In the proteins expressions, the EGFR, PI3K and AKT proteins expressions of lncRNA group were significantly inhibited and the P21 proteins expressions were significantly stimulated in the lncRNA groups compared with those of NC groups in Eca 109 and Kyse 150 cells.
Conclusion:
The lncRNA LINC00152 had anti-tumor effects on esophageal cancer in the Eca 109 and Kyse 150 cells, the mechanisms were relative with EGFR pathway.
Insights
Long non-coding RNA LINC00152 exhibits anti-tumor effects in esophageal cancer. It suppresses cell proliferation and impacts cell cycle regulation via the EGFR pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Esophageal cancer is a significant global health concern with limited effective therapeutic options.
- Long non-coding RNAs (lncRNAs) are emerging as critical regulators in various cancers, including esophageal cancer.
- Understanding the specific roles of lncRNAs like LINC00152 is crucial for developing novel treatment strategies.
Purpose of the Study:
- To elucidate the functional role of lncRNA LINC00152 in esophageal cancer.
- To investigate the underlying molecular mechanisms by which LINC00152 influences cancer progression.
- To evaluate the therapeutic potential of LINC00152 in esophageal cancer models.
Main Methods:
- Tissue samples: 30 pairs of esophageal cancer and adjacent normal tissues analyzed for LINC00152 expression using in situ hybridization (ISH) and RT-qPCR.
- Cell lines: Eca 109 and Kyse 150 cells were manipulated to overexpress lncRNA LINC00152.
- Functional assays: Cell proliferation (MTT), apoptosis, cell cycle (flow cytometry), and protein expression (Western blot) were assessed.
Main Results:
- Overexpression of lncRNA LINC00152 significantly suppressed esophageal cancer cell proliferation (P<0.05).
- LINC00152 overexpression notably enhanced cell apoptosis and promoted G1 phase arrest (P<0.05).
- Key proteins involved in cancer signaling, including EGFR, PI3K, and AKT, were inhibited, while P21 expression was stimulated by LINC00152.
Conclusions:
- Long non-coding RNA LINC00152 demonstrates significant anti-tumor activity against esophageal cancer cell lines (Eca 109 and Kyse 150).
- The anti-cancer mechanism of LINC00152 is associated with the regulation of the Epidermal Growth Factor Receptor (EGFR) signaling pathway.
- LINC00152 represents a potential therapeutic target for esophageal cancer treatment.
More Related Videos
Related Concept Videos
02:38Mitogens and the Cell Cycle
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...
01:12Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...