Expression of cathepsin D and E-cadherin in primary laryngeal cancers correlation with neck lymph node involvement

Paksoy, Mustafa; Hardal, Umit; Çakır, Çağlar

doi:10.1007/s00432-011-1007-z

Cited by 19 publications

(13 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Cathepsin D, a lysosomal aspartate proteolytic enzyme that is similar to cathepsin B, also plays an important role in invasion and metastasis of cancer. It is up-regulated in metastasis of some malignant tumors, including primary laryngeal cancers correlated with neck lymph node involvement [36], gastric cancer with lymphatic and/or blood vessel invasion [37], and breast cancer. Furthermore, Cheng et al [38] found that significant cathepsin D expression occurred in lymph node metastasis versus primary NPC and was significantly correlated with advanced clinical stage, recurrence, and lymph node and distant metastasis.…”

Section: Resultsmentioning

confidence: 99%

RETRACTED ARTICLE: Proteomic analysis on N, N′-dinitrosopiperazine-mediated metastasis of nasopharyngeal carcinoma 6-10B cells

Liu

Huang

et al. 2012

BMC Biochem

View full text Add to dashboard Cite

BackgroundNasopharyngeal carcinoma (NPC) has a high metastatic feature. N,N′-Dinitrosopiperazine (DNP) is involved in NPC metastasis, but its mechanism is not clear. The aim of this study is to reveal the pathogenesis of DNP-involved metastasis. 6-10B cells with low metastasis are from NPC cell line SUNE-1, were used to investigate the mechanism of DNP-mediated NPC metastasis.Results6-10B cells were grown in DMEM containing 2H4-L-lysine and 13C 6 15 N4-L-arginine or conventional L-lysine and L-arginine, and identified the incorporation of amino acid by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Labeled 6-10B cells were treated with DNP at 0 -18 μM to establish the non-cytotoxic concentration (NCC) range. NCC was 0 -10 μM. Following treatment with DNP at this range, the motility and invasion of cells were detected in vitro, and DNP-mediated metastasis was confirmed in the nude mice. DNP increased 6-10B cell metastasis in vitro and vivo. DNP-induced protein expression was investigated using a quantitative proteomic. The SILAC-based approach quantified 2698 proteins, 371 of which showed significant change after DNP treatment (172 up-regulated and 199 down-regulated proteins). DNP induced the change in abundance of mitochondrial proteins, mediated the status of oxidative stress and the imbalance of redox state, increased cytoskeletal protein, cathepsin, anterior gradient-2, and clusterin expression. DNP also increased the expression of secretory AKR1B10, cathepsin B and clusterin 6-10B cells. Gene Ontology and Ingenuity Pathway analysis showed that DNP may regulate protein synthesis, cellular movement, lipid metabolism, molecular transport, cellular growth and proliferation signaling pathways.ConclusionDNP may regulate cytoskeletal protein, cathepsin, anterior gradient-2, and clusterin expression, increase NPC cells motility and invasion, is involved NPC metastasis.

show abstract

Section: Resultsmentioning

confidence: 99%

RETRACTED ARTICLE: Proteomic analysis on N, N′-dinitrosopiperazine-mediated metastasis of nasopharyngeal carcinoma 6-10B cells

Liu

Huang

et al. 2012

BMC Biochem

View full text Add to dashboard Cite

show abstract

“…The expression of cathepsin D protein is known to promote the transport and metastasis of tumor cells (Paksoy et al, ). In this study, cathepsin D protein expression was significantly increased by treatment with E2 (about 1.3 times) and fludioxonil (about 1.2 times) at 72 h or in a time‐dependent manner compared to a control (0.1% DMSO).…”

Section: Resultsmentioning

confidence: 99%

Fludioxonil induced the cancer growth and metastasis via altering epithelial–mesenchymal transition via an estrogen receptor‐dependent pathway in cellular and xenografted breast cancer models

Kim

Jeon

et al. 2016

Environmental Toxicology

View full text Add to dashboard Cite

Fludioxonil is an antifungal agent used in agricultural applications that is present at measurable amounts in fruits and vegetables. In this study, the effects of fludioxonil on cancer cell viability, epithelial-mesenchymal transition (EMT), and metastasis were examined in MCF-7 clonal variant breast cancer cell (MCF-7 CV cells) with estrogen receptors (ERs). MCF-7 CV cells were cultured with 0.1% DMSO (control), 17β-estradiol (E2; 1 ×10 M, positive control), or fludioxonil (10 -10 M). MTT assay revealed that fludioxonil increased MCF-7 CV cell proliferation 1.2 to 1.5 times compared to the control, while E2 markedly increased the cell proliferation by about 3.5 times. When the samples were co-treated with ICI 182,780 (10 M), an ER antagonist, fludioxonil-induced cell proliferation was reversed to the level of the control. Protein levels of cyclin E1, cyclin D1, Snail, and N-cadherin increased in response to fludioxonil as the reaction to E2, but these increases were not observed when fludioxonil was administered with ICI 182,780. Moreover, the protein level of p21 and E-cadherin decreased in response to treatment with fludioxonil, but remained at the control level when co-treated with ICI 182,780. In xenografted mouse models transplanted with MCF-7 CV cells, fludioxonil significantly increased the tumor mass formation by about 2.5 times as E2 did when compared to vehicle (0.1% DMSO) during the experimental period (80 days). Immunohistochemistry revealed that the protein level of proliferating cell nuclear antigen (PCNA), Snail, and cathepsin D increased in response to fludioxonil as the reaction to E2. These results imply that fludioxonil may have a potential to induce growth or metastatic behaviors of breast cancer by regulation of the expression of cell cycle-, EMT-, and metastasis-related genes via the ER-dependent pathway. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1439-1454, 2017.

show abstract

“…Over-expression of N-cadherin is associated with an invasive capacity of breast tumor by increasing the interactions between tumor cells and stromal cells [ 39 ]. Based on the ability to induce the EMT process, E2 and CYP were found to promote the migration and invasion of Ishikawa cancer cells and to increase the protein expression of metastasis-related genes, such as Cathepsin D and MMP-9 [ 40 , 41 ], in the ER-dependent pathway. Therefore, these results indicate that CYP may induce metastatic processes of endometrial cancer cells including EMT, migration, and invasion, similar to E2.…”

Section: Discussionmentioning

confidence: 99%

3,3′-Diindolylmethane Suppressed Cyprodinil-Induced Epithelial-Mesenchymal Transition and Metastatic-Related Behaviors of Human Endometrial Ishikawa Cells via an Estrogen Receptor-Dependent Pathway

Kim

et al. 2018

IJMS

View full text Add to dashboard Cite

Cyprodinil (CYP) is a pyrimidine amine fungicide that has been extensively used in agricultural areas. 3,3 -Diindolylmethane (DIM) is a derivative of the dietary phytoestrogen, indole-3-carbinol (I3C), which is derived from cruciferous vegetables and considered to be a cancer-preventive phytonutrient agent. In this study, the effects of CYP and DIM were examined on the cell viability, invasion, and metastasis of human endometrial cancer cells, Ishikawa, via epithelial mesenchymal transition (EMT). CYP increased the level of cell viability of Ishikawa cells compared to DMSO as a control, as did E2. Ishikawa cells lost cell-to-cell contact and obtained a spindle-shaped or fibroblast-like morphology in response to the application of E2 or CYP by the cell morphology assay. In the cell migration and invasion assay, CYP enhanced the ability of migration and invasion of Ishikawa cells, as did E2. E2 and CYP increased the expressions of N-cadherin and Snail proteins, while decreasing the expression of E-cadherin protein as EMT-related markers. In addition, E2 and CYP increased the protein expressions of cathepsin D and MMP-9, metastasis-related markers. Conversely, CYP-induced EMT, cell migration, and invasion were reversed by fulvestrant (ICI 182,780) as an estrogen receptor (ER) antagonist, indicating that CYP exerts estrogenic activity by mediating these processes via an ER-dependent pathway. Similar to ICI 182,780, DIM significantly suppressed E2 and CYP-induced proliferation, EMT, migration, and invasion of Ishikawa cancer cells. Overall, the present study revealed that DIM has an antiestrogenic chemopreventive effect to withdraw the cancer-enhancing effect of E2 and CYP, while CYP has the capacity to enhance the metastatic potential of estrogen-responsive endometrial cancer.

show abstract

Expression of cathepsin D and E-cadherin in primary laryngeal cancers correlation with neck lymph node involvement

Cited by 19 publications

References 32 publications

RETRACTED ARTICLE: Proteomic analysis on N, N′-dinitrosopiperazine-mediated metastasis of nasopharyngeal carcinoma 6-10B cells

RETRACTED ARTICLE: Proteomic analysis on N, N′-dinitrosopiperazine-mediated metastasis of nasopharyngeal carcinoma 6-10B cells

Fludioxonil induced the cancer growth and metastasis via altering epithelial–mesenchymal transition via an estrogen receptor‐dependent pathway in cellular and xenografted breast cancer models

3,3′-Diindolylmethane Suppressed Cyprodinil-Induced Epithelial-Mesenchymal Transition and Metastatic-Related Behaviors of Human Endometrial Ishikawa Cells via an Estrogen Receptor-Dependent Pathway

Contact Info

Product

Resources

About