24小时热门版块排行榜

返回列表

【有奖交流】积极回复本帖子，参与交流，就有机会分得作者 pheiphei2025 的 1 个金币，回帖就立即获得 1 个金币，每人有 1 次机会

pheiphei2025

捐助贵宾 (初入文坛)

应助: 0 (幼儿园)
金币: 45
帖子: 4
在线: 30分钟
虫号: 36484786

[交流] 【深容SCI写作智能体】Abstract实测

【深容SCI写作智能体】Abstract实测

如需试用【深容SCI写作智能体】，请联系深容张老师：shenrongagent
[https://scioriginal.com]

上月深容推出了【深容SCI写作智能体】的Method，Introduction，Discussion智能体，写作质量非常高，全部真实参考文献，深受用户欢迎。
今天介绍的Abstract写作智能体，功能相对简单，根据用户提供的正文内容，快速起草摘要，同时输出结构式摘要和一体式摘要。
1. 用户输入正文内容：
2. 检索参考同类题材的摘要格式：
3. 输出结果Abstract。

智能体的写作质量非常高：

(1) Structured ABSTRACT
1) Background
Signal Transducer and Activator of Transcription 2 (STAT2) is well-known for its role in type I interferon (IFN-I) signaling, which is generally considered tumor-suppressive. However, its direct role in cancer, particularly colorectal cancer (CRC), remains underexplored. Given the critical involvement of immune and cytokine networks in CRC progression, elucidating STAT2's contribution is essential.
2) Methods
We analyzed TCGA-COAD datasets to assess STAT2 and IFNAR1 expression and patient survival. Human HCT116 and murine MC38 cell lines with STAT2 or IFNAR1 knockouts were generated using CRISPR\/Cas9 technology. Cell proliferation was measured in vitro using the CellTiter 96 assay. In vivo tumor growth was evaluated by subcutaneous injection of knockout and control cells into immunodeficient or immunocompetent mice. Western blot and qPCR analyses were performed to assess downstream signaling and gene expression changes.
3) Results
High STAT2 expression in TCGA-COAD tumors correlated with reduced patient survival, independent of IFNAR1 levels. STAT2 deletion impaired cell proliferation and tumor growth in both human and murine models, whereas IFNAR1 deletion did not. STAT2 KO cells exhibited reduced STAT1 activation but enhanced STAT3 phosphorylation, indicating distinct downstream signaling effects compared to IFNAR1 KO cells. These findings suggest that STAT2 promotes tumorigenicity through mechanisms distinct from canonical IFN-I signaling.
4) Conclusion
Our study reveals that STAT2 functions as a tumor-promoting factor in CRC, acting independently of IFNAR1-mediated IFN-I signaling. Targeting STAT2 or its downstream pathways may offer a novel therapeutic strategy for mitigating CRC progression.

---

(2) Integrated ABSTRACT
Signal Transducer and Activator of Transcription 2 (STAT2) is a key mediator of type I interferon (IFN-I) signaling, traditionally viewed as tumor-suppressive. However, its direct role in colorectal cancer (CRC) remains poorly defined, despite the critical influence of immune and cytokine networks on disease progression. To address this gap, we analyzed TCGA-COAD datasets and found that high STAT2 expression in CRC tumors correlated with reduced patient survival, independent of IFNAR1 levels. Using CRISPR\/Cas9 technology, we generated human HCT116 and murine MC38 cell lines with STAT2 or IFNAR1 knockouts. In vitro cell proliferation assays demonstrated that STAT2 deletion significantly impaired growth, whereas IFNAR1 deletion had no effect. In vivo studies in immunodeficient and immunocompetent mice confirmed that STAT2 KO cells formed smaller tumors compared to controls, while IFNAR1 KO cells did not differ significantly from wild-type cells. Western blot and qPCR analyses revealed that STAT2 deletion reduced STAT1 activation but enhanced STAT3 phosphorylation, indicating distinct downstream signaling effects compared to IFNAR1 KO cells. These findings suggest that STAT2 promotes tumorigenicity through mechanisms independent of canonical IFN-I signaling. Our study highlights STAT2 as a potential therapeutic target in CRC, offering new avenues for mitigating disease progression by targeting its pro-tumorigenic pathways.

以上这篇Abstract起草时间仅00:01:35

【深容SCI写作智能体】包括四大模块：Method智能体、Introduction智能体、Discussion智能体、Abstract智能体。
如需试用智能体，请徽售联系深容张老师：shenrongagent
[https://scioriginal.com]

#SCI论文 #科研 #实验 #博士 #投稿