Our new paper in @ScienceTM: In vivo #CRISPR activation screen identifies acyl-CoA binding protein as a driver of #bone #metastasis. Super excited by this discovery! @ACS_Research @AmericanCancer @MDAndersonNews .

RT @ScienceTM: Leveraging #CRISPR activation screens, researchers identify the lipid metabolism protein ACBP as a key driver of bone metast….

Grateful to my lab and collaborators for this super exciting milestone!.

Bone metastasis remains a major clinical challenge. By identifying ACBP as a metabolic driver of this process and demonstrating the efficacy of targeting lipid metabolism in preclinical models, our work opens new therapeutic avenues for halting bone metastasis.

🦴Our @ScienceTM study discovered ACBP as a metabolic driver of #BONE #metastasis. 🔬 Blocking fatty acid oxidation or inducing ferroptosis shuts down bone metastasis in vivo. 📰 @MDAndersonNews highlight:. @ACKoongMDPhD @DraettaG @CarinHagberg.

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Hiring Postdoctoral Fellows for Cancer Metastasis & Immunotherapy research in my lab at MD Anderson! #PostdocJobs #CancerResearch @MDAndersonNews Apply:

RT @Lo_Zanzi: #EveryCellIsAnImmuneCell! Deng @LiMaCancerLab &co show @NatMetabolism that during liver damage, LIFR drives production of CXC….

17-Kudos to the first author @Yalan_Deng and my entire team for their hard work and continued inspiration. Huge thanks to our collaborators, @Zhu_Lab, Michael Curran, and Chunru Lin, for sharing their resources and outstanding expertise.

16-Here, our findings reveal the mechanisms underlying injury-induced efflux of bone marrow neutrophils to the circulation and damaged liver, and uncover how reparative neutrophils signal to hepatocytes to proliferate in response to liver injury.

15-The contribution of neutrophils to tissue repair & regeneration is increasingly appreciated (PMIDs: 28983053; 33106668). Neutrophil recruitment can be divided into an early phase & an amplification phase. Likely, the later-recruited neutrophils participate in tissue repair.

14-Neutrophils are recruited to the site of tissue injury as early as 15-30 minutes and cover the necrotic area within a few hours. These early-recruited neutrophils are responsible for clearing necrotic tissue and cellular debris.

13-In this study, we uncovered a new role of cholesterol in the hepatic regenerative process, i.e., stimulating neutrophils to secrete HGF via its receptor ERR, which places cholesterol at the crossroads of metabolic regulation and immune regulation of liver regeneration.

12-Cholesterol, primarily produced by the liver and also acquired from certain foods, serves as a vital component of cell membranes as well as a precursor for the synthesis of bile acids, steroid hormones, and vitamin D.

11-We then found upon liver damage, hepatocytic LIFR promotes the production of CXCL1 and cholesterol in a STAT3-dependent manner to recruit and activate neutrophils. Via its receptor ERR, cholesterol stimulates neutrophils to produce HGF to accelerate hepatocyte proliferation.

10-After injury, the peak of hepatic neutrophil recruitment coincided with the upregulation of LIFR, cyclin D1, and cyclin A2 as well as the critical time point of liver regeneration. Neutrophil depletion demonstrated that LIFR-mediated liver regeneration is neutrophil-dependent.

9-Through CyTOF analysis and validation, we found that hepatocytic LIFR promotes neutrophil recruitment in liver regeneration models. Lipidomics analysis and validation showed that LIFR promotes cholesterol production after liver injury.

8-Interestingly, LIFR deficiency or overexpression did not affect hepatocyte proliferation ex vivo or in vitro, suggesting the involvement of other cell types in LIFR-facilitated liver regeneration in vivo.

7-In this study, liver-specific knockout of LIFR in mice impeded, whereas adenovirus-mediated delivery of LIFR accelerated liver injury repair and regeneration, revealing the role of a liver tumor suppressor in regeneration and a link between impaired tissue repair and cancer.

6-Intriguingly, we found that LIFR expression is frequently downregulated in liver cancer but is upregulated during the recovery phase after partial hepatectomy; after restoration of liver mass, LIFR expression goes back to the basal level.

5-The relationships between regeneration and cancer are complex. On the one hand, excessive regeneration may potentially induce tumorigenesis due to overgrowth. On the other hand, deficiency in regeneration may also promote cancer due to tissue damage that cannot be repaired.