Galectin-3 gene silencing inhibits migration and invasion of human tongue cancer cells in vitro via downregulating β-catenin

Zhang, Dong; Chen, Zhenggang; Liu, Shaohua; Dong, Zhao‐Ru; Dalin, Martin G.; Bao, Shaowen; Hu, Yingwei; Fang, Wei

doi:10.1038/aps.2012.150

Cited by 44 publications

(40 citation statements)

References 38 publications

(59 reference statements)

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“…A similar case exists for galectin-3, which displays, once more dual functionalities in cell proliferation. For instance, galectin-3 increases proliferation of breast, prostate, pancreatic and tongue tumors (47,(94)(95)(96)(97)(98). This might be due to the interaction of galectin-3 with the APC/Axin/β-catenin complex in the nucleus.…”

Section: Galectin (%) Cellular --------------------------------------mentioning

confidence: 99%

Intracellular galectins in cancer cells: Potential new targets for therapy

Vladoiu

Labrie

St‐Pierre

2014

International Journal of Oncology

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Abstract. Dysregulation of galectin expression is frequently observed in cancer tissues. Such an abnormal expression pattern often correlates with aggressiveness and relapse in many types of cancer. Because galectins have the ability to modulate functions that are important for cell survival, migration and metastasis, they also represent attractive targets for cancer therapy. This has been well-exploited for extracellular galectins, which bind glycoconjugates expressed on the surface of cancer cells. Although the existence of intracellular functions of galectins has been known for many years, an increasing number of studies indicate that these proteins can also alter tumor progression through their interaction with intracellular ligands. In fact, in some instances, the interactions of galectins with their intracellular ligands seem to occur independently of their carbohydrate recognition domain. Such findings call for a change in the basic assumptions, or paradigms, concerning the activity of galectins in cancer and may force us to revisit our strategies to develop galectin antagonists for the treatment of cancer.

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Section: Galectin (%) Cellular --------------------------------------mentioning

confidence: 99%

Intracellular galectins in cancer cells: Potential new targets for therapy

Vladoiu

Labrie

St‐Pierre

2014

International Journal of Oncology

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“…Despite advances in the therapeutic management of squamous cell carcinoma over the last few decades, the prognosis is still very poor due to local recurrence and metastasis [2-4]. This disappointing outcome, even with existing therapies, strongly suggests that novel targeted therapeutic agents are needed to improve the treatment of patients diagnosed with oral cancer.…”

Section: Introductionmentioning

confidence: 99%

“…RNAi is a post-transcriptional mechanism of gene silencing through chromatin remodeling, inhibition of protein translation, or direct mRNA degradation, which is ubiquitous in eukaryotic cells [6]. Along these lines, several recent studies have documented the successful downregulation of gene expression, resulting in increased apoptosis and decreased proliferation in many cancer cell lines [4,7]. Long-lasting RNAi-based gene silencing can be achieved using lentivirus-based expression systems, which drive the production of short hairpin RNAs (shRNAs) [8].…”

Section: Introductionmentioning

confidence: 99%

Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro

Zhang

Chen

et al. 2013

Cancer Cell Int

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BackgroundThe prognosis of oral squamous cell carcinoma is very poor due to local recurrence and metastasis. This study explores the molecular events involved in oral carcinoma with the goal of developing novel therapeutic strategies. The mitotic spindle is a complex mechanical apparatus required for the accurate segregation of sister chromosomes during mitosis. Spindle and kinetochore associated complex subunit 1 (SKA1) is a microtubule-binding subcomplex of the outer kinetochore that is essential for proper chromosome segregation. In recent years, much attention has been focused on determining how SKA proteins interact with each other, as well as their biological role in cancer cells. However, the precise role of SKA1 in oral carcinoma remains unknown.MethodsIn order to investigate the role of SKA1 in oral cancer, we employed lentivirus-mediated shRNA to silence SKA1 expression in the CAL-27 human oral adenosquamous carcinoma cell line.ResultsDepletion of SKA1 in CAL-27 cells significantly decreased cell proliferation, as determined by MTT and colony formation assays. These results strongly demonstrate that reduced SKA1 protein levels may cause inhibition of tumor formation. The shRNA-mediated depletion of SKA1 also led to G2/M phase cell cycle arrest and apoptosis.ConclusionThis is the first report to show that SKA1 plays an important role in the progression of oral adenosqamous carcinoma. Thus, silencing of SKA1 by RNAi might be a potential therapy for this disease.

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“…Further, exposure of WT Eos to eotaxin-1 in the presence of lactose to prevent binding of any secreted Gal-3 did not alter migration suggesting that Eos migration is likely to be regulated by intracellular rather than extracellular Gal-3, thus accounting for the decreased migration of Gal-3 -/- Eos. A role for intracellular Gal-3 in regulating cell migration has also been demonstrated in various cancer cells by silencing Gal-3 expression (Kim et al, 2010; Wang et al, 2012; Zhang et al, 2013). Overall, signaling involving intracellular Gal-3 and/or secreted Gal-3 bound to the cell surface of Eos appears to be essential for Eos trafficking under flow and migration.…”

Section: Discussionmentioning

confidence: 93%

Eosinophil-expressed galectin-3 regulates cell trafficking and migration

Ge¹,

Ha²,

Liu³

et al. 2013

Front. Pharmacol.

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Galectin-3 (Gal-3), a β galactoside-binding lectin, is implicated in the pathogenesis of allergic airway inflammation and allergen-challenged mice deficient in Gal-3 (Gal-3-/-) exhibit decreased airway recruitment of eosinophils (Eos). Gal-3 is expressed and secreted by several cell types and can thus function extracellularly and intracellularly to regulate a variety of cellular responses. We sought to determine the role of Eos-expressed Gal-3 in promoting Eos trafficking and migration in the context of allergic airway inflammation using bone marrow (BM)-derived Eos from wild-type (WT) and Gal-3-/- mice. Airway recruitment of Eos in acute (4 weeks) and chronic (8–12 weeks) allergen-challenged WT mice correlated with Gal-3 expression in the lungs. BM-derived Eos were found to express Gal-3 on the cell surface and secrete soluble Gal-3 when exposed to eotaxin-1. Compared to WT Eos, Gal-3-/- Eos exhibited significantly reduced rolling on vascular cell adhesion molecule 1 (VCAM-1) and decreased stable adhesion on intercellular adhesion molecule 1 (ICAM-1) under conditions of flow in vitro. Evaluation of cytoskeletal rearrangement demonstrated that relatively fewer adherent Gal-3-/- Eos undergo cell spreading and formation of membrane protrusions. In addition, cell surface expression of integrin receptor αM (CD11b) was lower in Gal-3-/- Eos, which is likely to account for their altered adhesive interactions with VCAM-1 and ICAM-1. Gal-3-/- Eos also exhibited significantly decreased migration toward eotaxin-1 compared to WT Eos irrespective of similar levels of CCR3 expression. Further, eotaxin-induced migration of WT Eos remained unaffected in the presence of lactose, suggesting a role for intracellular Gal-3 in regulating Eos migration. Overall, our findings indicate that Gal-3 expression in the lungs correlates with Eos mobilization during allergic airway inflammation and signaling involving intracellular Gal-3 and/or secreted Gal-3 bound to the cell surface of Eos appears to be essential for Eos trafficking under flow as well as for migration.

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Galectin-3 gene silencing inhibits migration and invasion of human tongue cancer cells in vitro via downregulating β-catenin

Cited by 44 publications

References 38 publications

Intracellular galectins in cancer cells: Potential new targets for therapy

Intracellular galectins in cancer cells: Potential new targets for therapy

Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro

Eosinophil-expressed galectin-3 regulates cell trafficking and migration

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