Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Department of Gastrointestinal Surgery, Changzhi People's Hospital, The Affiliated Hospital of Shanxi Medical University, Changzhi, China.
Mol Oncol. 2022 Oct;16(19):3509-3532. doi: 10.1002/1878-0261.13296. Epub 2022 Aug 11.
Adenocarcinoma is the most prevalent histological subtype of colorectal cancer (CRC), with mucinous colorectal adenocarcinoma (MCA) being a unique form. Although the mucinous subtype is known to elicit a worse response to chemotherapy and immunotherapy than the nonmucinous subtype, its pathogenesis remains poorly understood. Neurogenic locus notch homolog protein 3 (NOTCH3), a member of the NOTCH subfamilies, is highly expressed in CRC. In the past three decades, many studies have been performed evaluating the biological role of NOTCH3 in CRC. However, the precise activities of NOTCH3 in MCA, as well as the mechanisms involved in its transcriptional control, are yet to be elucidated. Our finding showed that the critical transcriptional regulatory factor transcription activator BRG1 (SMARCA4) directly binds to the intracellular domain of NOTCH3 to control transcriptional regulation. Moreover, RNA-sequencing results indicated a common targeting effect on the transcriptional activity of mucin-5AC (MUC5AC) and mucin-2 (MUC2) in CRC cells by NOTCH3 and SMARCA4. Furthermore, NOTCH3 was found to control the expressions of MUC5AC and MUC2 in a SMARCA4-dependent manner. MUC5AC and MUC2, which encode two secreted mucins, are located on chromosome 11p15.5, and are linked to the development of MCA. This finding suggests that the interaction between NOTCH3 and SMARCA4 may be involved in MCA differentiation by jointly targeting MUC5AC and MUC2. Patients with MCA are often treated in accordance with CRC guidelines. Determining the relationship between NOTCH3 and SMARCA4 by demonstrating their interactions in the pathophysiology of MCA could provide novel therapeutic targets and help identify potential prognostic markers for MCA.
腺癌是结直肠癌(CRC)最常见的组织学亚型,黏液性结直肠腺癌(MCA)是一种独特的形式。尽管已知黏液型比非黏液型对化疗和免疫治疗的反应更差,但其发病机制仍知之甚少。神经源性基因座 Notch 同源蛋白 3(NOTCH3)是 NOTCH 亚家族的成员,在 CRC 中高度表达。在过去的三十年中,已经进行了许多研究来评估 NOTCH3 在 CRC 中的生物学作用。然而,NOTCH3 在 MCA 中的精确活性以及其转录控制所涉及的机制仍有待阐明。我们的研究结果表明,关键的转录调节因子转录激活因子 BRG1(SMARCA4)直接与 NOTCH3 的细胞内结构域结合,以控制转录调节。此外,RNA-seq 结果表明,NOTCH3 和 SMARCA4 对 CRC 细胞中黏蛋白-5AC(MUC5AC)和黏蛋白-2(MUC2)的转录活性有共同的靶向作用。此外,NOTCH3 被发现以依赖于 SMARCA4 的方式控制 MUC5AC 和 MUC2 的表达。编码两种分泌型黏蛋白的 MUC5AC 和 MUC2 位于 11p15.5 染色体上,与 MCA 的发生有关。这一发现表明,NOTCH3 和 SMARCA4 之间的相互作用可能通过共同靶向 MUC5AC 和 MUC2 参与 MCA 分化。MCA 患者通常根据 CRC 指南进行治疗。通过证明 NOTCH3 和 SMARCA4 在 MCA 病理生理学中的相互作用,可以确定它们之间的关系,这可能为 MCA 提供新的治疗靶点,并有助于确定潜在的 MCA 预后标志物。