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驱动永生化细胞和癌细胞三维生长的基因。

Genes driving three-dimensional growth of immortalized cells and cancer.

作者信息

Basu Mukta, Xiao Jin-Fen, Kailasam Mani Saravana Kumar, Qu Fangyuan, Lin Yongqi, Duex Jason, Ye Huihui, Neang Vanessa, Theodorescu Dan

机构信息

Department of Urology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

出版信息

Cell Death Dis. 2025 Jun 10;16(1):442. doi: 10.1038/s41419-025-07719-5.

Abstract

Unchecked growth in three-dimensions (3D) in culture is a key feature of immortalized cells on the path to malignant transformation and hence a potential target phenotype for prevention. Also, expression of genes driving this process, but not that of 2D growth, would likely be more specific to cancer development and their inhibition would be less toxic to normal cells, many of which can grow in 2D but rarely in 3D culture. To define such genes, we compared CRISPR depletion screens performed in HBLAK, a spontaneously immortalized, non-tumorigenic human urothelial cell line, grown in 2D to those in 3D. Using the CRISPR Bassik DTKP (drug target kinase phosphatase) deletion library targeting 2,333 genes, we identified 85 genes which were specifically lost in 3D cultures. Prioritizing hits to those associated with bladder cancer in patients provided us with a set of 11 genes. Only one gene, MAPK1 remained relevant if a human pan-cancer criteria was applied. Single gene in vitro validation confirmed that MAPK1 inhibition was specific to 3D growth. We also found that MAPK1 depletion led to significant growth reductions in human tumor xenografts in vivo. Inhibition of MAPK1 by Ulixertinib, an orally active MAPK1 inhibitor, led to human bladder cancer growth inhibition in both 3D in vitro and in vivo models. In summary, screening for genes specifically driving 3D growth in immortalized cells may provide targets for both prevention and early therapy in bladder and other cancers while potentially limiting therapeutic toxicity.

摘要

在培养中不受控制的三维(3D)生长是永生化细胞在恶性转化过程中的一个关键特征,因此是预防的一个潜在靶标表型。此外,驱动这一过程的基因表达,而非二维生长相关基因的表达,可能对癌症发展更具特异性,抑制这些基因对正常细胞的毒性可能更小,因为许多正常细胞可以在二维中生长,但很少能在三维培养中生长。为了确定此类基因,我们比较了在二维培养的HBLAK(一种自发永生化、无致瘤性的人尿道上皮细胞系)中进行的CRISPR基因敲除筛选与在三维培养中的筛选结果。使用靶向2333个基因的CRISPR Bassik DTKP(药物靶标激酶磷酸酶)缺失文库,我们鉴定出85个在三维培养中特异性缺失的基因。根据与膀胱癌患者相关的情况对筛选结果进行排序,为我们提供了一组11个基因。如果应用人类泛癌标准,只有一个基因MAPK1仍然相关。单基因体外验证证实,抑制MAPK1对三维生长具有特异性。我们还发现,敲除MAPK1会导致体内人肿瘤异种移植物的生长显著减少。口服活性MAPK1抑制剂Ulixertinib对MAPK1的抑制导致人膀胱癌在三维体外和体内模型中均出现生长抑制。总之,筛选在永生化细胞中特异性驱动三维生长的基因可能为膀胱癌和其他癌症的预防和早期治疗提供靶点,同时可能限制治疗毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3f/12152191/221789e3e64c/41419_2025_7719_Fig1_HTML.jpg

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