Galectin-9 expression links to malignant potential of cervical squamous cell carcinoma

Liang, Meiyan; Ueno, Masaki; Oomizu, Souichi; Arikawa, Tomohiro; Shinonaga, Rika; Zhang, Shulan; Yamauchi, Akira; Hirashima, Mitsuomi

doi:10.1007/s00432-008-0352-z

Cited by 60 publications

(57 citation statements)

References 29 publications

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“…Friedrichs et al (2007) reported that galectin-3 and-9 are the most abundantly expressed galectins in Madin-Darby canine kidney (MDCK) cells, a commonly used general model for epithelial cells, which comprise epithelium. Liang et al (2008) observed potent immunostaining for cytoplasmic Galectin-9 in normal squamous epithelial cells of the cervix which appears to involve the entire epithelium while Cada et al (2009) reported basal and suprabasal presence of Galectin-9 in the epidermis. More relevantly, Fik et al (2013) described expression of Galectin-9 exclusively at the basal layer of normal oral epithelium.…”

Section: Discussionmentioning

confidence: 99%

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Changed Expression of E-cadherin and Galectin-9 in Oral Squamous Cell Carcinomas but Lack of Potential as Prognostic Markers

Kallarakkal²,

Abraham³

2014

Asian Pacific Journal of Cancer Prevention

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Background: The survival rate for oral squamous cell carcinoma (OSCC) has remained generally unchanged in the past three decades, underlining the need for more biomarkers to be developed to aid prognostication and effective management. The prognostic potential of E-cadherin expression in OSCCs has been variable in previous studies while galectin-9 expression has been correlated with improved prognosis in other cancers. The aim of the present study was to investigate the expression of galectin-9 and E-cadherin in OSCC and their potential as prognostic biomarkers. Materials and Methods: E-cadherin and Galectin-9 expression was examined by immunohistochemistry in 32 cases of OSCC of the buccal mucosa (13 with and 19 without lymph node metastasis), as well as 6 samples of reactive lesions and 5 of normal buccal mucosa. Results: The expression of E-cadherin in OSCC was significantly lower than the control tissues but galectin-9 expression was conversely higher. Median E-cadherin HSCOREs between OSCCs positive and negative for nodal metastasis were not significantly different. Mean HSCOREs for galectin-9 in OSCC without lymph node metastasis (127.7±81.8) was higher than OSCC with lymph node metastasis (97.9±62.9) but this difference was not statistically significant. Conclusions: E-cadherin expression is reduced whilst galectin-9 expression is increased in OSCC. However, the present results suggest that E-cadherin and galectin-9 expression may not be useful as prognostic markers for OSCC.

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Section: Discussionmentioning

confidence: 99%

“…H-SCORE is a summation of the proportion of cell staining at each intensity multiplied by the intensity of the staining (Berchuck et al, 1989) represented by the following formula (Kitawaki et al, 1999;Liang et al, 2008):…”

Section: Ihc Staining Evaluationmentioning

confidence: 99%

Changed Expression of E-cadherin and Galectin-9 in Oral Squamous Cell Carcinomas but Lack of Potential as Prognostic Markers

Kallarakkal²,

Abraham³

2014

Asian Pacific Journal of Cancer Prevention

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“…12,13 Loss of expression of LGALS9 is also associated with metastatic progression in various epithelial cancers, including breast and colorectal cancer. [14][15][16][17][18] Taken together, this suggests that loss of LGALS9 promotes a metastatic tumor phenotype. Conversely, treatment of LGALS9 deficient monolayers with exogenous recombinant LGALS9 (rLGALS9) restores epithelial polarity.…”

Section: Introductionmentioning

confidence: 88%

The epithelial polarity regulator LGALS9/galectin-9 induces fatal frustrated autophagy in KRAS mutant colon carcinoma that depends on elevated basal autophagic flux

et al. 2015

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Section: Discussionmentioning

confidence: 99%

“…For example, studies have shown interaction between the gal-9 on lymphocytes and the Tim-3 on APCs may have a positive role in DC maturation process, 13,22 while ligation of the gal-9 on APCs and the Tim-3 on lymphocytes have an opposite role as to tune down the immune response. 15,35,36,46,49 The function of the various gal-9 ϩ immuneregulatory cells seen in mice with advanced AML on the generation and function of CD8 ϩ T cells in this model is of interest and will require extensive future investigations beyond the scope of this study to clearly define the role of each.The additive effects of combined in vivo blockade of the PD-1/PDL1 and Tim-3/gal-9 in reducing AML disease burden and prolonging survival was demonstrated in studies in which Tim3-Fc fusion protein and anti-PDL1 mAb were given to WT mice or anti-PDL1 mAb was given to gal-9 KO mice. The latter resulted in a more pronounced long-term survival than the former, which may be because of the incomplete blockade at sites of AML disease likely achieved with a fusion protein compared with the obligatory blockade of a KO mouse.…”

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confidence: 99%

Coexpression of Tim-3 and PD-1 identifies a CD8+ T-cell exhaustion phenotype in mice with disseminated acute myelogenous leukemia

Zhou

Munger

Veenstra

et al. 2011

Blood

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Tumor-associated immune suppression can lead to defective T cell-mediated antitumor immunity. Here, we identified a unique phenotype of exhausted T cells in mice with advanced acute myelogenous leukemia (AML). This phenotype is characterized by the coexpression of Tim-3 and PD-1 on CD8 ؉ T cells in the liver, the major first site of AML metastases. PD-1 and Tim-3 coexpression increased during AML progression. PD-1 ؉ Tim-3 ؉ CD8 ؉ T cells were deficient in their ability to produce IFN-␥, TNF-␣, and IL-2 in response to PD-1 ligand (PDL1) and Tim-3 ligand (galectin-9) expressing AML cells. PD-1 knockout (KO), which were partially resistant to AML challenge, up-regulated Tim-3 during AML progression and such Tim-3 ؉ PD-1-KO CD8 ؉ T cells had reduced cytokine production. Galectin-9 KO mice were more resistant to AML, which was associated with reduced T-regulatory cell accumulation and a modest induction of PD-1 and Tim-3 expression on CD8 ؉ T cells. Whereas blocking the PD-1/ PDL1 or Tim-3/galectin-9 pathway alone was insufficient to rescue mice from AML lethality, an additive effect was seen in reducing-albeit not eliminating-both tumor burden and lethality when both pathways were blocked. Therefore, combined PD-1/PDL1 and Tim-3/galectin-9 blockade may be beneficial in preventing CD8 ؉ T-cell exhaustion in patients with hematologic malignancies such as advanced AML. (Blood. 2011;117(17):4501-4510) Introduction T-cell exhaustion, a state of T-cell dysfunction characterized by diminished cytokine production, impaired killing, and hypoproliferation, was first characterized in the settings of chronic lymphocytic choriomeningitis virus (LCMV) infection. 1,2-5 Since its discovery, the process of T-cell exhaustion has been of intense interest and has been the subject of study in viral infections such as hepatitis C virus 2,6 and HIV, 3,7 as well as in tumor models. 8,9,10,11 Cell-surface antigen determinants such as program death-1 (PD-1), CTLA-4, and, in some instances, CD28 (eg, hepatitis C viral infection) can be used to identify antigen-specific T cells that are at an exhaustion stage. 4 T-cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) is a type I membrane glycoprotein and its expression can be found on terminally differentiated Th1 cells and innate immune cells. [12][13][14] is its only confirmed Tim-3 ligand to date, 15,16 although it is known that Tim-3 can also bind to certain carbohydrate moieties. 17 Ligation of Tim-3 on T cells and gal-9 inhibits Th1 responses and plays an important role in infection, autoimmunity, peripheral tolerance, and inflammation. 14,[18][19][20][21] In addition to its negative regulatory role in dampening the immune system, a recent report showed a synergistic effect of Tim-3 signaling and lipopolysaccharide in producing proinflammatory cytokines by naive dendritic cells (DCs) and monocytes, 22 indicating a dual role of the Tim-3 signaling pathway at a different phase of immune responses.Studies have demonstrated a strong correlation between PD-1 and Tim-3 coexpressi...

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Galectin-9 expression links to malignant potential of cervical squamous cell carcinoma

Abstract: The present results suggest that decreased Gal-9 expression is inversely associated with malignant potential or differentiation of cervical CIN and SCC as a differentiation biomarker.

Cited by 60 publications

References 29 publications

Changed Expression of E-cadherin and Galectin-9 in Oral Squamous Cell Carcinomas but Lack of Potential as Prognostic Markers

Changed Expression of E-cadherin and Galectin-9 in Oral Squamous Cell Carcinomas but Lack of Potential as Prognostic Markers

The epithelial polarity regulator LGALS9/galectin-9 induces fatal frustrated autophagy in KRAS mutant colon carcinoma that depends on elevated basal autophagic flux

Coexpression of Tim-3 and PD-1 identifies a CD8+ T-cell exhaustion phenotype in mice with disseminated acute myelogenous leukemia

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