Serum LECT2 level as a prognostic indicator in acute liver failure

Sato, Yoshinobu; Watanabe, Hidenori; Kameyama, Hitoshi; Kobayashi, Takahiro; Yamamoto, Shuichi; Takeishi, Toshiyuki; Hirano, Keisuke; Oya, Hiroshi; Nakatsuka, Hideki; Watanabe, Takayuki; Kokai, H.; Yamagoe, S.; Suzuki, Kazuo; Oya, Kiyofumi; Kojima, Kensuke; Hatakeyama, K.

doi:10.1016/j.transproceed.2004.07.007

Cited by 41 publications

(30 citation statements)

References 3 publications

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“…Studies using this ELISA protocol reported the presence of LECT2 levels in human serum or plasma in the range of 1-15 ng/mL (18)(19)(20). Recently, Ando et al reported LECT2 levels of 19.7 ± 3.4 ng/mL in heparinized plasma from healthy volunteers with the conventional ELISA protocol (21).…”

Section: Discussionmentioning

confidence: 96%

Increased serum leukocyte cell-derived chemotaxin 2 (LECT2) levels in obesity and fatty liver

et al. 2013

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Section: Discussionmentioning

confidence: 96%

Increased serum leukocyte cell-derived chemotaxin 2 (LECT2) levels in obesity and fatty liver

et al. 2013

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“…17 This protein is synthesized by hepatocytes and has been associated with repair and cell growth after damage. 16,[32][33][34] Accumulating evidence suggests that LECT2 is a pleiotropic protein, as are many cytokines. LECT2 has an important role in neuronogenesis, and its mutation is the major cause of primary microencephaly.…”

Section: Discussionmentioning

confidence: 99%

The tumor suppressor function of LECT2 in human hepatocellular carcinoma makes it a potential therapeutic target

Ong¹,

Tan²,

Wang³

et al. 2011

Cancer Gene Ther

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Vascular invasion is one of the clinicopathologic features that are associated with early recurrence of human hepatocellular carcinoma (HCC). In this study, we have employed high-density Affymetrix oligonucleotide GeneChips (Affymetrix, Santa Clara, CA) to compare the expression profiles of HCC with and without vascular invasion. Data mining of the gene expression database established revealed that leukocyte cell-derived chemotaxin-2 (LECT2) transcripts were downregulated in HCC patients with vascular invasion. Expression of LECT2 in human HCC biopsies was significantly reduced (Po0.0001, fold change ¼ À7.2) when compared with non-tumorous adjacent liver tissues. The reduction of LECT2 expression was significantly correlated with the early recurrent and poor prognosis of the patient (P ¼ 0.024). To validate the ability of LECT2 to repress the growth of HCC, an adenoviral vector encoding the secreted human LECT2 (AdLECT2) was introduced into the human HCC cell lines Hep3B and PLC/PRF/5, which do not express endogenous LECT2. Over-expression of LECT2 resulted in the significant inhibition of in vitro migration and invasion of the AdLECT2-transfected HCC cells. Additionally, over-expression of AdLECT2 in subcutaneous Hep3B tumor xenografts in athymic nude mice resulted in significant inhibition of tumor growth (Po0.05). In summary, our data not only demonstrated that LECT2 is a candidate prognostic marker of human HCC, but also that therapeutic strategies targeting LECT2 expression is a promising therapy for human HCC.

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“…Following an overnight fast, venous blood samples were taken from each patient. Serum levels of LECT2 were measured by an Ab-Match ASSEMBLY Human LECT2 kit (MBL Co.) (26,27). …”

Section: Human Clinical Studiesmentioning

confidence: 99%

LECT2 Functions as a Hepatokine That Links Obesity to Skeletal Muscle Insulin Resistance

et al. 2014

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Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell–derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance.

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Serum LECT2 level as a prognostic indicator in acute liver failure

Cited by 41 publications

References 3 publications

Increased serum leukocyte cell-derived chemotaxin 2 (LECT2) levels in obesity and fatty liver

Increased serum leukocyte cell-derived chemotaxin 2 (LECT2) levels in obesity and fatty liver

The tumor suppressor function of LECT2 in human hepatocellular carcinoma makes it a potential therapeutic target

LECT2 Functions as a Hepatokine That Links Obesity to Skeletal Muscle Insulin Resistance

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