An Lkb1-Sik axis suppresses tumor growth and controls differentiation [RNA-Seq]

Background: LKB1 is among the most frequently altered tumor suppressors in lung adenocarcinoma. Despite being implicated in the regulation of a variety of cellular processes, the mechanisms by which LKB1 constrains lung tumor growth and progression remains an area of intense investigation. Purpose: To determine the extent of overlap in terms of the transcriptomic states arising from either Lkb1 deletion or Sik-targeting within cancer cells isolated from genetically engineered mouse models of oncogenic Kras-driven lung adenocarcinoma Approach: Cancer cells sorted from mouse lung tumors of defined genotypes were profiled by RNA-seq. Results: A strong overlap existed between Lkb1-deficient and Sik-targeted cancer cells both at the gene and pathways levels. Conclusions: Given the strong transcriptional overlap, loss of either Lkb1 or Sik appear to be functionally related. RNA-seq of WT, Lkb1 deletion or Sik-targeted mouse lung cancer cells.

背景：LKB1是肺腺癌中最频发突变的肿瘤抑制基因之一。尽管其参与调控多种细胞生物学过程，但LKB1限制肺肿瘤生长与进展的具体分子机制仍是当前研究的热点领域。目的：本研究旨在明确在致癌KRAS驱动的肺腺癌基因工程小鼠模型中分离的癌细胞内，Lkb1缺失与Sik靶向干预所诱导的转录组状态的重叠程度。方法：对从特定基因型小鼠肺肿瘤中分选得到的癌细胞开展RNA-seq转录组谱分析。结果：在基因与通路层面，Lkb1缺陷型与Sik靶向干预的癌细胞之间存在显著的转录组重叠。结论：鉴于二者存在显著的转录组重叠，Lkb1或Sik的缺失在功能上具有相关性。本数据集包含野生型（Wild Type, WT）、Lkb1缺失型及Sik靶向干预型小鼠肺癌细胞的RNA-seq测序数据。