. 2023 Aug 8;35(8):1457-1473.e13.

doi: 10.1016/j.cmet.2023.05.009. Epub 2023 Jun 16.

Molecular mechanisms of snoRNA-IL-15 crosstalk in adipocyte lipolysis and NK cell rejuvenation

Yaohua Zhang¹, Zilong Zhao¹, Lisa A Huang¹, Yuan Liu², Jun Yao¹, Chengcao Sun¹, Yajuan Li¹, Zhao Zhang³, Youqiong Ye³, Fei Yuan⁴, Tina K Nguyen¹, Nikhil Reddy Garlapati¹, Andrew Wu¹, Sergey D Egranov¹, Abigail S Caudle⁵, Aysegul A Sahin⁶, Bora Lim⁷, Laura Beretta¹, George A Calin⁸, Dihua Yu⁹, Mien-Chie Hung¹⁰, Michael A Curran¹¹, Katayoun Rezvani¹², Boyi Gan¹³, Zhi Tan¹⁴, Leng Han¹⁵, Chunru Lin¹⁶, Liuqing Yang¹⁷

Affiliations

¹ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
² Center for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX, USA.
³ Department of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston McGovern Medical School, Houston, TX 77030, USA.
⁴ Center for Drug Discovery, Department of Pathology & Immunology, Baylor College of Medicine, Houston, TX 77030, USA.
⁵ Department of Breast Surgical Oncology, Division of Surgery, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
⁶ Department of Pathology, Division of Pathology and Laboratory Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
⁷ Oncology/Medicine, Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA.
⁸ Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Center for RNA Interference and Non-Coding RNAs, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
⁹ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
¹⁰ Graduate Institute of Biomedical Sciences, Institute of Biochemistry and Molecular Biology, Research Center for Cancer Biology, Cancer Biology and Precision Therapeutics Center, and Center for Molecular Medicine, China Medical University, Taichung 406, Taiwan.
¹¹ Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Immunology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
¹² Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Stem Cell Transplantation and Cellular Therapy, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
¹³ Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Experimental Radiation Oncology, Division of Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
¹⁴ Center for Drug Discovery, Department of Pathology & Immunology, Baylor College of Medicine, Houston, TX 77030, USA; Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: zhi.tan@bcm.edu.
¹⁵ Center for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX, USA; Brown Center for Immunotherapy, School of Medicine, Indiana University, Indianapolis, IN 46202, USA; Department of Biostatistics and Health Data Science, School of Medicine, Indiana University, Indianapolis, IN 46202, USA. Electronic address: lenghan@iu.edu.
¹⁶ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: clin2@mdanderson.org.
¹⁷ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Center for RNA Interference and Non-Coding RNAs, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: lyang7@mdanderson.org.

PMID: 37329887
PMCID: PMC10712687
DOI: 10.1016/j.cmet.2023.05.009

Molecular mechanisms of snoRNA-IL-15 crosstalk in adipocyte lipolysis and NK cell rejuvenation

Yaohua Zhang et al. Cell Metab. 2023.

. 2023 Aug 8;35(8):1457-1473.e13.

doi: 10.1016/j.cmet.2023.05.009. Epub 2023 Jun 16.

Authors

Affiliations

¹ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
² Center for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX, USA.
³ Department of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston McGovern Medical School, Houston, TX 77030, USA.
⁴ Center for Drug Discovery, Department of Pathology & Immunology, Baylor College of Medicine, Houston, TX 77030, USA.
⁵ Department of Breast Surgical Oncology, Division of Surgery, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
⁶ Department of Pathology, Division of Pathology and Laboratory Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
⁷ Oncology/Medicine, Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA.
⁸ Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Center for RNA Interference and Non-Coding RNAs, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
⁹ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
¹⁰ Graduate Institute of Biomedical Sciences, Institute of Biochemistry and Molecular Biology, Research Center for Cancer Biology, Cancer Biology and Precision Therapeutics Center, and Center for Molecular Medicine, China Medical University, Taichung 406, Taiwan.
¹¹ Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Immunology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
¹² Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Stem Cell Transplantation and Cellular Therapy, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
¹³ Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Experimental Radiation Oncology, Division of Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
¹⁴ Center for Drug Discovery, Department of Pathology & Immunology, Baylor College of Medicine, Houston, TX 77030, USA; Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: zhi.tan@bcm.edu.
¹⁵ Center for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX, USA; Brown Center for Immunotherapy, School of Medicine, Indiana University, Indianapolis, IN 46202, USA; Department of Biostatistics and Health Data Science, School of Medicine, Indiana University, Indianapolis, IN 46202, USA. Electronic address: lenghan@iu.edu.
¹⁶ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: clin2@mdanderson.org.
¹⁷ Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Center for RNA Interference and Non-Coding RNAs, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: lyang7@mdanderson.org.

PMID: 37329887
PMCID: PMC10712687
DOI: 10.1016/j.cmet.2023.05.009

Abstract

Obesity, in which the functional importance of small nucleolar RNAs (snoRNAs) remains elusive, correlates with risk for many cancer types. Here, we identify that the serum copies of adipocyte-expressed SNORD46 correlate with body mass index (BMI), and serum SNORD46 antagonizes interleukin-15 (IL-15) signaling. Mechanically, SNORD46 binds IL-15 via G11, and G11A (a mutation that significantly enhances binding affinity) knockin drives obesity in mice. Functionally, SNORD46 blocks IL-15-induced, FER kinase-dependent phosphorylation of platelet glycoprotein 4 (CD36) and monoglyceride lipase (MGLL) in adipocytes, leading to inhibited lipolysis and browning. In natural killer (NK) cells, SNORD46 suppresses the IL-15-dependent autophagy, leading to reduced viability of obese NK. SNORD46 power inhibitors exhibit anti-obesity effects, concurring with improved viability of obese NK and anti-tumor immunity of CAR-NK cell therapy. Hence, our findings demonstrate the functional importance of snoRNAs in obesity and the utility of snoRNA power inhibitors for antagonizing obesity-associated immune resistance.

Keywords: adipocyte; autophagy; interleukin-15; lipase; natural killer cells; obesity; small nucleolar RNA.

PubMed Disclaimer

Conflict of interest statement

Declaration of interests M.A.C. reports grants and personal fees from ImmunoGenesis, Inc. and personal fees from Alligator Bioscience, Inc.; ImmunOS, Inc.; Oncoresponse, Inc.; Nurix, Inc.; Aptevo, Inc.; Kineta, Inc.; Xencor, Inc.; Agenus, Inc.; Adagene, Inc.; and Astrazeneca, Inc. outside the submitted work. K.R. and the University of Texas MD Anderson Cancer Center have an institutional financial conflict of interest with Takeda Pharmaceutical and Affimed GmbH. K.R. participates on the Scientific Advisory Board for GemoAb, AvengeBio, Virogin Biotech, GSK, Caribou Biosciences, Navan Technologies, and Bayer. B.G. is an inventor on patent applications involving targeting ferroptosis in cancer therapy and reports personal fees from Guidepoint Global, Cambridge Solutions, and NGM Bio.

Figures

**Figure 1.. *SNORD46* correlates with BMI and immune resistance**
(A) Heatmap of snoRNA expression of indicated human serum samples. (B) Copy number of *SNORD46* (left) or U6 (right) in serum of human donors with BMI < 25, 30-40, or > 40 (n = 128, 128, 126 donors). (C and D) Northern blotting using indicated probes of indicated human serum (C), or human adipose tissues as indicated (D). (E) Copy number of *SNORD46* (left) or U6 (right) in serum with indicated BMI, without or with exercise (0, ≥ 420 min/week), n = 18 donor per group, one-way ANOVA. (F) Pearson correlation between *SNORD46* copy number and exercise time of donors with BMI < 30 (left) or BMI > 30 (right), n = 18 (BMI < 30), 18 (BMI > 30) donor, Fisher’s exact test. (G and H) The spearman’s correlation of *SNORD46* expression and immune cell type enrichment (G) and immunophenoscore (IPS) (H) in 28 cancer types. (I and J) Representative multi-IHC images (I) and statistical analysis of CD8 and NCAM1 (J) of breast cancer tissues from serum *SNORD46*-high or *SNORD46*-low breast cancer patients. Scale bars, 100 μm. Error bars, SD, n = 15, 14 tissues, unpaired Student’s t-test.

Figure 2.. C/EBPβ regulates the transcriptional expression of *SNORD46*
(A) Top: graphic illustration of PICh-MS determination using *SNORD46* promoter region. Bottom: heatmap of the PICh-MS protein identification using scramble, *SNORD46* promoter or telomere sequence as indicated. R: biological repeat. (B) Relative expression of *SNORD46*, normalized by U6 snRNA of differentiated human adipocyte harboring indicated siRNAs. Error bars, SD, n = 7 independent experiments, one-way ANOVA. (C) Copy number of *SNORD46* (left) or U6 (right) in supernatant of C/EBPβ parental (Par.) or knockout (KO) adipocytes expressing indicated expression vectors. Error bars, SD, n = 26 donors, one-way ANOVA. (D) ChIP-qPCR detection of the C/EBPβ occupancy on *LINK-A*, *SNORD46* or *RPS8* promoter regions of differentiated human adipocytes expressing indicated expression constructs. Error bars, SD, n = 5 independent experiments, two-way ANOVA. (E) Immunoblotting (IB) detection of indicated proteins in adipose tissues from chow or HFD-fed mice with or without treadmill exercise (TE). (F and G) Serum *Snord46* (F) or U6 (G) copy number in wild-type mice challenged with chow or HFD followed with or without treadmill exercise. Error bars, SD, n = 21 mice per group, one-way ANOVA. (H) IB detection of indicated proteins in differentiated human adipocytes supernatant upon indicated stimuli. (I) Copy number of *SNORD46* (left) or U6 (right) in differentiated human adipocytes supernatant upon indicated stimuli. Error bars, SD, n = 26 donors, one-way ANOVA.

**Figure 3.. *SNORD46* physically interact with IL15**
(A) Heatmap of the protein identification score for biotinylated Scramble, *SNORD46* or *miR-20a* pull-down. R: biological replicate. (B) IB detection (left) and autoradiography (right) of IL15 CLIP assay using human (H) or mice (M) serum. Blue box: RNA-protein complex extracted for the following sanger sequencing. (C) Summary of *SNORD46* sequence responsible for IL15 binding. The chromatin sequences corresponding to RNA (negative-stranded) and RNA motif bound by IL15 are shown. (D) Competition binding assay to determine K_d of the interaction between His-tagged IL15 and biotinylated-*SNORD46* wild-type or mutants. Unlabeled IL15 serve as the competitor. Error bars, SD, n = 3 independent experiments. *miR-20a* was included as a negative control. (E) Number of peptides recovered from LiP-MS of IL15 incubated with scramble or *SNORD46* RNA. x-axis: amino acid position of full-length IL15. (F) Competition binding assay to determine K_d of the interaction between His-tagged IL15 wild-type or mutants and biotinylated-*SNORD46*. Unlabeled *SNORD46* serve as competitor. Error bars, SD, n = 3 independent experiments. (G) Computational modeling of *SNORD46*–IL15 interaction. Magenta cartoon: *SNORD46*; Cyan cartoon: IL15; Magenta stick: G11; Cyan stick: D8 and N65. (H) G11A mutation of *SNORD46* strengthens the interaction with IL15. Green cartoon: *SNORD46*; Cyan cartoon: IL15; Green stick: A11; Cyan stick: D8 and N65. (I and J) RIP assay using differentiated human adipocytes harboring IL15 sgRNAs (I), or *SNORD46* sgRNAs (J) and *Adipoq*-driven expression of indicated mutants. Error bars, SD, n = 26 donors, one-way ANOVA.

**Figure 4.. *SNORD46* G11A drives obesity**
(A) Schematic of CRISPR-Cas9 method used to generate *SNORD46*^G11A/G11A mice. (B and C) Body weight measurement of female (B) or male (C) *Snord46*^WT/WT, *Snord46*^WT/G11A or *Snord46*^G11A/G11A mice. Error bars, SD, n = 7 mice, one-way ANOVA. (**D-H**) Representative images of lean and fat tissues (D), quantification of male (left) or female (right) body weight (E), lean weight (F), fat weight (G), and fat percentage (H) by the dual energy x-ray absorptiometry imaging system from *Snord46*^WT/WT or *Snord46*^G11A/G11A mice. Error bars, SD, n = 5 mice, Student’s t-test. (I) Representative H&E and Oil Red O staining of indicated tissues from *Snord46*^WT/WT or *Snord46*^G11A/G11A mice. Scale bars, 100 μm. (J) Statistical analysis of Oil Red O staining intensity of liver sections from *Snord46*^WT/WT or *Snord46*^G11A/G11A mice. Error bars, SD, n = 8 mice, Student’s t-test. (K and L) CLAMS measurement of oxygen consumption (VO₂) in male (K) or female (L) *Snord46*^WT/WT or *Snord46*^G11A/G11A mice. Error bars, SD, n = 4, 4 mice, two-way ANOVA. (M) Glucose tolerance tests (GTTs) of male *Snord46*^WT/WT or *Snord46*^G11A/G11A mice at the indicated time points. Error bars, SD, n = 8, 5 mice, Student’s t-test for each time point.

**Figure 5.. IL15 triggers FER-medicated signaling cascades in adipocytes to regulates the enzymatic activities of CD36 and MGLL**
(A) Identification of biotinylated IL15-associated proteins in *Snord46*^WT/WT or *Snord46*^G11A/G11A tissues as indicated. Protein scores are shown. (B) IL15 pull-down followed by IB detection of indicated proteins in mouse adipocytes with or without IL15 stimulation. (C) Ni-NTA pull-down using indicated recombinant proteins and biotinylated RNA oligonucleotides, followed by IB detection using indicated antibodies. (D) IB detection of indicated proteins in NK cells or differentiated human adipocytes (HAd) with or without IL15 stimulation. (E and F) IB detection of indicated proteins in WT, *Il2rb*-deficient or *Snord46*^G11A/G11A adipocytes with or without IL15 stimulation. (**G-I**) Measurement of intracellular TG (G), intracellular NEFA (H), or extracellular NEFA (I) concentration of differentiated WT, *Il2rb*^−/−or *Snord46* ^G11A/G11A adipocytes with or without IL15 stimulation. Error bars, SD, n = 8 animals per experimental group, one-way ANOVA. (J) Oxygen consumption rate (OCR) across time for WT, *Il2rb*^−/− and *Snord46*^G11A/G11A mouse adipocytes with or without IL15 stimulation. Dot lines indicate the addition of mitochondrial inhibitors (oligomycin; FCCP; antimycin A/rotenone) (n = 8 wells of adipocytes, error bars: SD). (K and L) Measurement of intracellular TG (K) and intracellular NEFA (L) levels in *MGLL*-proficient or -deficient differentiated human adipocytes expressing indicated expression constructs with or without IL15 stimulation. Error bars, SD, n = 24 donors, two-way ANOVA.

**Figure 6.. *SNORD46* power inhibitors antagonize obesity**
(A) Heatmap of the protein identification score for biotinylated Scramble, *SNORD46* or *miR-20a* pull-down in the presence of indicated power inhibitors. R: biological replicate. (B) Northernblot of *SNORD46* in human serum treated with indicated power inhibitors or antibodies. (C) IB detection of proteins associated with biotinylated RNA (wild-type and indicated mutants) in human serum treated with indicated power inhibitors. (D) IB detection of indicated proteins in differentiated human adipocytes collected from donors with BMI < 25, 30-40, or > 40 and treated with IL15 and/or indicated power inhibitors. (E and F) Measurement of intracellular TG (E) or intracellular NEFA (F) levels in differentiated human adipocytes collected from donors with BMI < 25 (n = 24), 30-40 (n= 19), or > 40 (n = 17) and treated with indicated power inhibitors with or without IL15 stimulation. Error bars, SD, two-way ANOVA. (G) Left, representative images; right, body weight measurement of *Snord46*^G11A/G11A mice treated with scramble (Scr), *Snord46* power inhibitor (pi), Orlistat or Liraglutide as indicated. Error bars, SD, n = 5 mice per group, one-way ANOVA. (H) Representative H&E and Oil Red O staining of liver or WAT (left) and statistical analysis of staining intensities of liver sections (right) from *Snord46*^G11A/G11A mice treated with scramble or *Snord46* power inhibitor. Scale bars, 100 μm. Error bars, SD, n= 9, 8 mice, Student’s t-test.

**Figure 7.. *SNORD46* power inhibitors restore the anti-tumor immunity of CAR-NK cells under obesity**
(A) Volcano presentation of the transcription profiling of NK cells isolated from donors with obesity (n = 5) or healthy donors (n = 4). (B) Heatmap of the expression of Autophagy gene signature of NK cells isolated from donors with obesity (n = 5) or healthy donors (n = 4). (C) Immunofluorescent labeling using indicated antibodies in NK cells isolated from PBMC of healthy donors (BMI < 25) or donors with obesity (BMI > 35). Scale bars, 20 μm. Error bars, SD, n = 5, 5 donors, Student’s t-test. (D) Percentage of NK cells viability (left) and IC₅₀ determination of NK cells viability (right) of BMI < 25, or BMI > 35 donors. Error bars, SD, n = 3 independent experiment, Student’s t-test. (E) Percentage of NK cells viability (left) and IC₅₀ determination of NK cells viability (right) of *Snord46* ^WT/WT or *Snord46* ^G11A/G11A mice. Error bars, SD, n = 3 independent experiment, Student’s t-test. (F) Percentage of NK cells viability (left) and IC₅₀ determination of NK cells viability (right) of BMI < 25, or BMI > 35 donors treated with scramble or *SNORD46* power inhibitor. Error bars, SD, n = 3 independent experiment, one-way ANOVA. (G) Percentage of NK cells viability (left) and IC₅₀ determination of NK cells viability (right) of *Snord46* ^WT/WT or *Snord46* ^G11A/G11A mice treated with scramble or *Snord46* power inhibitor. Error bars, SD, n = 3 independent experiment, one-way ANOVA. (H) Top: schematic illustration of CAR-NK cells in HT-29 xenograft tumors. Bottom: tumor volume measurement of HT-29 tumor of chow (left) or HFD-fed animals (right) upon CAR-NK and indicated powder inhibitor treatment. Error bars, SD, n = 5 mice per group, one-way ANOVA. (I) Top: schematic illustration of CAR-NK cells in MDA-MB-231 xenograft tumors. Bottom: tumor volume measurement of MDA-MB-231 tumor of chow (left) or HFD-fed animals (right) upon CAR-NK and indicated power inhibitor treatment. Error bars, SD, n = 5 mice per group, one-way ANOVA. (J and K) Percentage of CD56⁺ NK cells isolated from HT-29 tumor (J) or MDA-MB-231 tumor (K) of chow or HFD-fed animals upon indicated treatment. Error bars, SD, n = 5 mice per group, one-way ANOVA.

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Molecular mechanisms of snoRNA-IL-15 crosstalk in adipocyte lipolysis and NK cell rejuvenation

Affiliations

Molecular mechanisms of snoRNA-IL-15 crosstalk in adipocyte lipolysis and NK cell rejuvenation

Authors

Affiliations

Abstract

Conflict of interest statement

Figures

References

Publication types

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Grants and funding

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Full Text Sources

Molecular Biology Databases