基质MTHFD2驱动纤维化-炎症微环境促进肿瘤生长与免疫逃逸

数据集获取

源站：https://ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313754

标准获取流程：

1. 访问源站链接，注册/登录账号；
2. 进入数据集详情页，按页面指引申请权限或直接下载；
3. 部分平台提供 SDK，例如：
   • OpenDataLab: pip install openxlab 后 openxlab.dataset.get(...)
   • ModelScope: pip install modelscope 后 modelscope download
   • 天池: 登录后页面提供直链下载
     以源站「数据下载/使用文档」页面为准。

数据说明

Cancer-associated fibroblasts (CAFs) are key drivers of fibrosis and immune suppression; however, the molecular basis linking these processes remains unclear. Here, we identified methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) as a stromal metabolic regulator that integrates fibrotic activation with inflammatory signaling. Fibrotic cues, such as TGF-β and matrix stiffening, induced MTHFD2 expression in fibroblasts, whereas its knockdown reduced α-SMA expression and IL-6/IL-8 secretion. Overexpression enhanced IL-6 production, even without fibrotic stimulation. Single-cell RNA-seq data from non-small-cell lung cancer revealed elevated MTHFD2 levels across CAF subsets, independent of their myofibroblastic or inflammatory states. Mechanistically, MTHFD2 sustained NAD+–ROS signaling and induced mitochondrial stress with DNA release, activating the cGAS–STING–NF-κB pathway and promoting IL-6-dependent PD-L1 expression. Fibroblast-specific deletion of MTHFD2 suppressed tumor growth and reduced PD-L1 expression in vivo. These findings define MTHFD2 as a stromal metabolic–inflammatory switch and highlight stromal metabolism as a potential therapeutic target in desmoplastic cancers.

数据加载示例（图像类）

from PIL import Image
import glob, os

files = (glob.glob(os.path.join(path, "**", "*.png"), recursive=True)
       + glob.glob(os.path.join(path, "**", "*.jpg"), recursive=True)
       + glob.glob(os.path.join(path, "**", "*.tif"), recursive=True))
print("图像文件数:", len(files))
img = Image.open(files[0]); print("尺寸/模式:", img.size, img.mode)

# torchvision Dataset 方式:
# from torchvision import datasets
# ds = datasets.ImageFolder(path)  # 要求 子目录=类别

目录组织与标注格式以源站说明和下载后实际文件为准。