We identified an lncRNA, LINC01503, which is increased in SCC cells compared with non-tumor cells. Increased expression of LINC01503 promotes ESCC cell proliferation, migration, invasion, and growth of xenograft tumors. It might be developed as a biomarker of aggressive SCCs in patients.
LPS-induced TNFα factor (LITAF) is a multiple functional molecule whose sequence is identical to small integral membrane protein of the lysosome/late endosome (SIMPLE). LITAF was initially identified as a transcription factor that activates transcription of proinflammatory cytokine in macrophages in response to LPS. Mutations of the LITAF gene are associated with a genetic disease, called Charcot-Marie-Tooth syndrome. Recently we have reported that mRNA levels of LITAF and tumor necrosis factor superfamily member 15 (TNFSF15) are upregulated by AMPK. The present study further assesses their biological functions. Thus, we show that AICAR, a pharmacological activator of AMPK, increases the abundance of LITAF and TNFSF15 in the LNCaP and C4-2 prostate cancer cells, which is abrogated by shRNA or dominant negative mutant of AMPK α1 subunit. Our data further demonstrate that AMPK activation upregulates the transcription of LITAF. Intriguingly, silencing LITAF by shRNA enhances proliferation, anchorage-independent growth of these cancer cells, and tumor growth in xenograft model. In addition, our study reveals that LITAF mediates the effect of AMPK by binding to a specific sequence in the promoter region. Furthermore, we show that TNFSF15 remarkably inhibits the growth of prostate cancer cells and bovine aortic endothelial cells in vitro with a more potent effect toward the latter. In conjuncture, intratumor injection of TNFSF15 significantly reduces the size of tumors and number of blood vessels and induces changes characteristic of tumor cell differentiation. Therefore, our studies for the first time establish the regulatory axis of AMPK-LITAF-TNFSF15. They also suggest that LITAF may function as a tumor suppressor.
In the version of this article initially published, the citation of Figure 3 in the second paragraph of the third subsection (Chromatin: the nexus of phenotype and the environment) is incorrect. That should cite Figure 2, as follows: "From an evolutionary perspective, two extreme models of how such complexity might be generated and regulated can be envisaged 95 (Fig. 2). " The error has been corrected in the HTML and PDF versions of the article.Erratum: Sall1 is a transcriptional regulator defining microglia identity and function In the HTML version of this article initially published, the scale bar was missing from the inset in the top right image in Figure 2d; the bottom left plot in Figure 2e was incorrectly a duplicate of the adjacent plot at right; and the designations in Figure 4b (Sall1 f l and Sall1 creER/fl ) should have been Sall1 fl/fl and Sall1 CreER/fl (respectively). Also, the arrows in the designations above and below the plots in Supplementary Figure 3b were rendered as boxes; these should have been as follows: Sall1 +/+ →Cx3cr1 CreER -iDTR and Sall1 GFP/+ →Cx3cr1 CreER -iDTR. Finally, in Supplementary Figure 4f, the red (Ki67 + ) cells in the right set of images were not visible. These errors have been corrected for the HTML version of this article.
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