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Article ; Online: Bitter melon extract suppresses metastatic breast cancer cells (MCF-7 cells) growth possibly by hindering glucose uptake.

Kakuturu, Abhinav / Choi, Heeyun / Noe, Leah G / Scherer, Brianna N / Sharma, Bikram / Khambu, Bilon / Bhetwal, Bhupal P

microPublication biology

2023 Volume 2023

Abstract: Breast cancer is one of the most commonly diagnosed cancers among women, however the complete cure for metastatic breast cancer is lacking due to poor prognosis. There has been an increasing trend of dietary modifications including consumption of natural ...

Abstract	Breast cancer is one of the most commonly diagnosed cancers among women, however the complete cure for metastatic breast cancer is lacking due to poor prognosis. There has been an increasing trend of dietary modifications including consumption of natural food for the prevention of cancer. One of the popular natural foods is bitter melon. Bitter melon grows in tropical and subtropical areas. Some of the beneficial effects of bitter melon towards disease including cancer have been reported at the whole body/organismal level. However, specific cellular mechanisms by which bitter melon exerts beneficial effects in breast cancer are lacking. In this study, we used a human metastatic breast cancer cell line, MCF-7 cell, to study if bitter melon alters glucose clearance from the culture medium. We co-cultured MCF-7 cells with bitter melon extract in the presence and absence of supplemented insulin and subsequently measured MCF-7 cells viability. In this study, we report a noble finding that bitter melon extract exerts cytotoxic effects on MCF-7 cells possibly via inhibition of glucose uptake. Our findings show that insulin rescues MCF-7 cells from the effects of bitter melon extract.
Language	English
Publishing date	2023-09-05
Publishing country	United States
Document type	Journal Article
ISSN	2578-9430
ISSN (online)	2578-9430
DOI	10.17912/micropub.biology.000961
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Article: Therapeutic regulation of autophagy in hepatic metabolism.

Byrnes, Katherine / Blessinger, Sophia / Bailey, Niani Tiaye / Scaife, Russell / Liu, Gang / Khambu, Bilon

Acta pharmaceutica Sinica. B

2021 Volume 12, Issue 1, Page(s) 33–49

Abstract: Metabolic homeostasis requires dynamic catabolic and anabolic processes. Autophagy, an intracellular lysosomal degradative pathway, can rewire cellular metabolism linking catabolic to anabolic processes and thus sustain homeostasis. This is especially ... ...

Abstract	Metabolic homeostasis requires dynamic catabolic and anabolic processes. Autophagy, an intracellular lysosomal degradative pathway, can rewire cellular metabolism linking catabolic to anabolic processes and thus sustain homeostasis. This is especially relevant in the liver, a key metabolic organ that governs body energy metabolism. Autophagy's role in hepatic energy regulation has just begun to emerge and autophagy seems to have a much broader impact than what has been appreciated in the field. Though classically known for selective or bulk degradation of cellular components or energy-dense macromolecules, emerging evidence indicates autophagy selectively regulates various signaling proteins to directly impact the expression levels of metabolic enzymes or their upstream regulators. Hence, we review three specific mechanisms by which autophagy can regulate metabolism: A) nutrient regeneration, B) quality control of organelles, and C) signaling protein regulation. The plasticity of the autophagic function is unraveling a new therapeutic approach. Thus, we will also discuss the potential translation of promising preclinical data on autophagy modulation into therapeutic strategies that can be used in the clinic to treat common metabolic disorders.
Language	English
Publishing date	2021-07-28
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	2211-3835
ISSN	2211-3835
DOI	10.1016/j.apsb.2021.07.021
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Article ; Online: Role of High-Mobility Group Box-1 in Liver Pathogenesis.

Khambu, Bilon / Yan, Shengmin / Huda, Nazmul / Yin, Xiao-Ming

International journal of molecular sciences

2019 Volume 20, Issue 21

Abstract: High-mobility group box 1 (HMGB1) is a highly abundant DNA-binding protein that can relocate to the cytosol or undergo extracellular release during cellular stress or death. HMGB1 has a functional versatility depending on its cellular location. While ... ...

Abstract	High-mobility group box 1 (HMGB1) is a highly abundant DNA-binding protein that can relocate to the cytosol or undergo extracellular release during cellular stress or death. HMGB1 has a functional versatility depending on its cellular location. While intracellular HMGB1 is important for DNA structure maintenance, gene expression, and autophagy induction, extracellular HMGB1 acts as a damage-associated molecular pattern (DAMP) molecule to alert the host of damage by triggering immune responses. The biological function of HMGB1 is mediated by multiple receptors, including the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs), which are expressed in different hepatic cells. Activation of HMGB1 and downstream signaling pathways are contributing factors in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), and drug-induced liver injury (DILI), each of which involves sterile inflammation, liver fibrosis, ductular reaction, and hepatic tumorigenesis. In this review, we will discuss the critical role of HMGB1 in these pathogenic contexts and propose HMGB1 as a bona fide and targetable DAMP in the setting of common liver diseases.
MeSH term(s)	Animals ; HMGB1 Protein/metabolism ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Receptor for Advanced Glycation End Products/metabolism ; Signal Transduction ; Toll-Like Receptors/metabolism
Chemical Substances	AGER protein, human ; HMGB1 Protein ; HMGB1 protein, human ; Receptor for Advanced Glycation End Products ; Toll-Like Receptors
Language	English
Publishing date	2019-10-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20215314
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Article ; Online: Hepatic Autophagy Deficiency Remodels Gut Microbiota for Adaptive Protection via FGF15-FGFR4 Signaling.

Yan, Shengmin / Khambu, Bilon / Chen, Xiaoyun / Dong, Zheng / Guo, Grace / Yin, Xiao-Ming

Cellular and molecular gastroenterology and hepatology

2020 Volume 11, Issue 4, Page(s) 973–997

Abstract: Background & aims: The functions of the liver and the intestine are closely tied in both physiological and pathologic conditions. The gut microbiota (GM) often cause deleterious effects during hepatic pathogenesis. Autophagy is essential for liver ... ...

Abstract	Background & aims: The functions of the liver and the intestine are closely tied in both physiological and pathologic conditions. The gut microbiota (GM) often cause deleterious effects during hepatic pathogenesis. Autophagy is essential for liver homeostasis, but the impact of hepatic autophagy function on liver-gut interaction remains unknown. Here we investigated the effect of hepatic autophagy deficiency (Atg5Δhep) on GM and in turn the effect of GM on the liver pathology. Methods: Fecal microbiota were analyzed by 16S sequencing. Antibiotics were used to modulate GM. Cholestyramine was used to reduce the enterohepatic bile acid (BA) level. The functional role of fibroblast growth factor 15 (FGF15) and ileal farnesoid X receptor (FXR) was examined in mice overexpressing FGF15 gene or in mice given a fibroblast growth factor receptor-4 (FGFR4) inhibitor. Results: Atg5Δhep causes liver injury and alterations of intestinal BA composition, with a lower proportion of tauro-conjugated BAs and a higher proportion of unconjugated BAs. The composition of GM is significantly changed with an increase in BA-metabolizing bacteria, leading to an increased expression of ileal FGF15 driven by FXR that has a higher affinity to unconjugated BAs. Notably, antibiotics or cholestyramine treatment decreased FGF15 expression and exacerbated liver injury. Consistently, inhibition of FGF15 signaling in the liver enhances liver injury. Conclusions: Deficiency of autophagy function in the liver can affect intestinal environment, leading to gut dysbiosis. Surprisingly, such changes provide an adaptive protection against the liver injury through the FGF15-FGFR4 signaling. Antibiotics use in the condition of liver injury may thus have unexpected adverse consequences via the gut-liver axis.
MeSH term(s)	Acute Lung Injury/etiology ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/prevention & control ; Animals ; Autophagy ; Autophagy-Related Protein 5/physiology ; Bile Acids and Salts/metabolism ; Dysbiosis/complications ; Female ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Gastrointestinal Microbiome ; Homeostasis ; Male ; Mice ; Mice, Knockout ; Receptor, Fibroblast Growth Factor, Type 4/genetics ; Receptor, Fibroblast Growth Factor, Type 4/metabolism
Chemical Substances	Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Bile Acids and Salts ; fibroblast growth factor 15, mouse ; Fibroblast Growth Factors (62031-54-3) ; Fgfr4 protein, mouse (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1)
Language	English
Publishing date	2020-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2020.10.011
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Article: NRF2 transcriptionally regulates Caspase-11 expression to activate HMGB1 release by Autophagy-deficient hepatocytes.

Khambu, Bilon / Cai, Genxiang / Liu, Gang / Bailey, Niani Tiaye / Mercer, Arissa A / Baral, Kamal / Ma, Michelle / Chen, Xiaoyun / Li, Yu / Yin, Xiao-Ming

Cell death discovery

2023 Volume 9, Issue 1, Page(s) 270

Abstract: Injury or stress can induce intracellular translocation and release of nuclear HMGB1, a DAMP molecule known to participate in inflammation and other pathological processes. Active release of HMGB1 from stimulated macrophages can be mediated by ... ...

Abstract	Injury or stress can induce intracellular translocation and release of nuclear HMGB1, a DAMP molecule known to participate in inflammation and other pathological processes. Active release of HMGB1 from stimulated macrophages can be mediated by inflammasomes, which cleave Gasdermin D to form pores on cytoplasmic membranes. We previously had shown that active release of HMGB1 from autophagy deficient hepatocytes also depended on the inflammasome but how the inflammasome was activated was not known. Here we report that persistent activation of transcription factor NRF2 under the autophagy deficient condition led to transcriptional upregulation of Caspase-11 expression, which could then activate the CASPASE-1inflammasome. Using chromatin immunoprecipitation (CHIP) and luciferase-based reporter assays, we show that NRF2 directly binds to the Caspase-11 promoter and transcriptionally increase the expression of Caspase-11. Genetic deletion of Caspase-11 in autophagy-deficient livers represses the release of HMGB1 and its pathological consequence, ductular cell proliferation. Consistently, deletion of NLRP3, which can activate CASPASE-1 mediated inflammasomes under other types of signals, did not prevent HMGB1 release and ductular cell proliferation in autophagy deficient livers. Surprisingly, while cleavage of GASDEMIN D occurred in autophagy-deficient livers its deletion did not prevent the HMGB1 release, suggesting that CASPASE-11-mediated inflammasome activation may also engage in a different mechanism for HMGB1 release by the autophagy deficient hepatocytes. Collectively, this work reveals the novel role of NRF2 in transcriptional upregulation of Caspase-11 and in inflammasome activation to promote active release of HMGB via a non-Gasdermin D mediated avenue.
Language	English
Publishing date	2023-07-28
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-023-01495-x
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Article: Impaired hepatic autophagy exacerbates hepatotoxin induced liver injury.

Byrnes, Katherine / Bailey, Niani Tiaye / Baral, Kamal / Mercer, Arissa / Joshi, Spandan / Wahby, Nickol / Rorison, Tyler / Liu, Gang / Yin, Xiao-Ming / Khambu, Bilon

Cell death discovery

2023 Volume 9, Issue 1, Page(s) 71

Abstract: Hepatotoxins activate the hepatic survival pathway, but it is unclear whether impaired survival pathways contribute to liver injury caused by hepatotoxins. We investigated the role of hepatic autophagy, a cellular survival pathway, in cholestatic liver ... ...

Abstract	Hepatotoxins activate the hepatic survival pathway, but it is unclear whether impaired survival pathways contribute to liver injury caused by hepatotoxins. We investigated the role of hepatic autophagy, a cellular survival pathway, in cholestatic liver injury driven by a hepatotoxin. Here we demonstrate that hepatotoxin contained DDC diet impaired autophagic flux, resulting in the accumulation of p62-Ub-intrahyaline bodies (IHBs) but not the Mallory Denk-Bodies (MDBs). An impaired autophagic flux was associated with a deregulated hepatic protein-chaperonin system and significant decline in Rab family proteins. Additionally, p62-Ub-IHB accumulation activated the NRF2 pathway rather than the proteostasis-related ER stress signaling pathway and suppressed the FXR nuclear receptor. Moreover, we demonstrate that heterozygous deletion of Atg7, a key autophagy gene, aggravated the IHB accumulation and cholestatic liver injury. Conclusion: Impaired autophagy exacerbates hepatotoxin-induced cholestatic liver injury. The promotion of autophagy may represent a new therapeutic approach for hepatotoxin-induced liver damage.
Language	English
Publishing date	2023-02-21
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-023-01368-3
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Article ; Online: Analysis of Autophagy for Liver Pathogenesis.

Huda, Nazmul / Zou, Hui / Yan, Shengmin / Khambu, Bilon / Yin, Xiao-Ming

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1880, Page(s) 481–489

Abstract: The autophagy pathway in hepatocytes is well characterized. Autophagy plays a critical role in the normal function of the liver. A growing number of studies suggest that there is a mechanistic relationship between autophagy and the pathogenesis of human ... ...

Abstract	The autophagy pathway in hepatocytes is well characterized. Autophagy plays a critical role in the normal function of the liver. A growing number of studies suggest that there is a mechanistic relationship between autophagy and the pathogenesis of human diseases including liver diseases. Here we focus on the methods assessing the level of lipids, lipid peroxidation, and lipophagy in the liver, which would be particularly relevant to the study of fatty liver diseases.
MeSH term(s)	Animals ; Autophagy/physiology ; Biological Assay/instrumentation ; Biological Assay/methods ; Cell Culture Techniques/instrumentation ; Cell Culture Techniques/methods ; Cell Line ; Fatty Liver/pathology ; Hepatocytes/metabolism ; Lipid Droplets/metabolism ; Lipid Metabolism/physiology ; Lipids/analysis ; Liver/metabolism ; Liver/pathology ; Mice ; Microscopy, Confocal/instrumentation ; Microscopy, Confocal/methods ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism
Chemical Substances	Lipids ; Reactive Oxygen Species
Language	English
Publishing date	2019-01-04
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8873-0_30
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Article ; Online: Autophagy, Metabolism, and Alcohol-Related Liver Disease: Novel Modulators and Functions.

Yan, Shengmin / Khambu, Bilon / Hong, Honghai / Liu, Gang / Huda, Nazmul / Yin, Xiao-Ming

International journal of molecular sciences

2019 Volume 20, Issue 20

Abstract: Alcohol-related liver disease (ALD) is caused by over-consumption of alcohol. ALD can develop a spectrum of pathological changes in the liver, including steatosis, inflammation, cirrhosis, and complications. Autophagy is critical to maintain liver ... ...

Abstract	Alcohol-related liver disease (ALD) is caused by over-consumption of alcohol. ALD can develop a spectrum of pathological changes in the liver, including steatosis, inflammation, cirrhosis, and complications. Autophagy is critical to maintain liver homeostasis, but dysfunction of autophagy has been observed in ALD. Generally, autophagy is considered to protect the liver from alcohol-induced injury and steatosis. In this review, we will summarize novel modulators of autophagy in hepatic metabolism and ALD, including autophagy-mediating non-coding RNAs (ncRNAs), and crosstalk of autophagy machinery and nuclear factors. We will also discuss novel functions of autophagy in hepatocytes and non-parenchymal hepatic cells during the pathogenesis of ALD and other liver diseases.
MeSH term(s)	Animals ; Autophagy ; Gene Expression Regulation ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Diseases, Alcoholic/genetics ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; RNA, Untranslated/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism
Chemical Substances	RNA, Untranslated ; Receptors, Cytoplasmic and Nuclear
Language	English
Publishing date	2019-10-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20205029
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Article ; Online: Hepatic senescence, the good and the bad.

Huda, Nazmul / Liu, Gang / Hong, Honghai / Yan, Shengmin / Khambu, Bilon / Yin, Xiao-Ming

World journal of gastroenterology

2019 Volume 25, Issue 34, Page(s) 5069–5081

Abstract: Gradual alterations of cell's physiology and functions due to age or exposure to various stresses lead to the conversion of normal cells to senescent cells. Once becoming senescent, the cell stops dividing permanently but remains metabolically active. ... ...

Abstract	Gradual alterations of cell's physiology and functions due to age or exposure to various stresses lead to the conversion of normal cells to senescent cells. Once becoming senescent, the cell stops dividing permanently but remains metabolically active. Cellular senescence does not have a single marker but is characterized mainly by a combination of multiple markers, such as, morphological changes, expression of cell cycle inhibitors, senescence associated β-galactosidase activity, and changes in nuclear membrane. When cells in an organ become senescent, the entire organism can be affected. This may occur through the senescence-associated secretory phenotype (SASP). SASP may exert beneficial or harmful effects on the microenvironment of tissues. Research on senescence has become a very exciting field in cell biology since the link between age-related diseases, including cancer, and senescence has been established. The loss of regenerative and homeostatic capacity of the liver over the age is somehow connected to cellular senescence. The major contributors of senescence properties in the liver are hepatocytes and cholangiocytes. Senescent cells in the liver have been implicated in the etiology of chronic liver diseases including cirrhosis and hepatocellular carcinoma and in the interference of liver regeneration. This review summarizes recently reported findings in the understanding of the molecular mechanisms of senescence and its relationship with liver diseases.
MeSH term(s)	Aging/physiology ; Bile Ducts, Intrahepatic/cytology ; Cellular Senescence ; Hepatocytes/pathology ; Humans ; Liver/cytology ; Liver/pathology ; Liver Diseases/pathology ; Liver Regeneration/physiology
Language	English
Publishing date	2019-09-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v25.i34.5069
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Article ; Online: Relevance of autophagy to fatty liver diseases and potential therapeutic applications.

Yan, Shengmin / Huda, Nazmul / Khambu, Bilon / Yin, Xiao-Ming

Amino acids

2017 Volume 49, Issue 12, Page(s) 1965–1979

Abstract: Autophagy is an evolutionarily conserved lysosome-mediated cellular degradation program. Accumulating evidence shows that autophagy is important to the maintenance of liver homeostasis. Autophagy involves recycling of cellular nutrients recycling as well ...

Abstract	Autophagy is an evolutionarily conserved lysosome-mediated cellular degradation program. Accumulating evidence shows that autophagy is important to the maintenance of liver homeostasis. Autophagy involves recycling of cellular nutrients recycling as well as quality control of subcellular organelles. Autophagy deficiency in the liver causes various liver pathologies. Fatty liver disease (FLD) is characterized by the accumulation of lipids in hepatocytes and the dysfunction in energy metabolism. Autophagy is negatively affected by the pathogenesis of FLD and the activation of autophagy could ameliorate steatosis, which suggests a potential therapeutic approach to FLD. In this review, we will discuss autophagy and its relevance to liver diseases, especially FLD. In addition, we will discuss recent findings on potential therapeutic applications of autophagy modulators for FLD.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy/physiology ; Biomarkers/analysis ; Fatty Liver/metabolism ; Fatty Liver/physiopathology ; Fatty Liver/therapy ; Humans ; Lipid Metabolism/physiology ; Liver/cytology ; Liver/metabolism ; Liver/physiopathology ; Lysosomes/metabolism ; Molecular Targeted Therapy ; Signal Transduction
Chemical Substances	Biomarkers
Language	English
Publishing date	2017-05-06
Publishing country	Austria
Document type	Journal Article ; Review
ZDB-ID	1121341-3
ISSN	1438-2199 ; 0939-4451
ISSN (online)	1438-2199
ISSN	0939-4451
DOI	10.1007/s00726-017-2429-y
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