Biologic Effect of Human Hepatocyte Growth-Factor on Human Gastric-Carcinoma Cell-Lines

Yokozaki, Hiroshi; Ito, Masumi; W, Yasui; Kyo, Eikai; Kuniyasu, Hiroki; Kitadai, Yasuhiko; Tsubouchi, Hironobu; Daikuhara, Yasushi; Tahara, Eiichi

doi:10.3892/ijo.3.1.89

Cited by 5 publications

(6 citation statements)

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“…Many studies have shown that disruption of cell‐to‐cell adhesion, enzymatic degradation of extracellular matrix, and acceleration of cell motility are important for invasion20, 21. We have reported previously the importance of hepatocyte growth factor/scatter factor receptor c‐ met , E‐cadherin1–3, 22, and type IV collagenase (MMP‐2/‐9)4–6, 23 in the development and metastasis of various carcinomas.…”

Section: Discussionmentioning

confidence: 99%

“…Cell adhesion, cell motility, and the production of matrix proteinase are essential for invasion. We have reported previously that overexpression of hepatocyte growth factor/scatter factor receptor c‐ met , linked with reduced expression of E‐cadherin, is closely correlated with the invasive activity of gastric cancer1–3. Reduced E‐cadherin expression and overexpression of type IV collagenase (MMP‐2/‐9) are also correlated with invasive and metastatic activity of prostate4, lung5, and pancreatic cancer6.…”

Section: Introductionmentioning

confidence: 99%

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Expression of receptors for advanced glycation end‐products (RAGE) is closely associated with the invasive and metastatic activity of gastric cancer

Kuniyasu

Oue

Wakikawa

et al. 2001

The Journal of Pathology

290

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The receptor for advanced glycation end-products (RAGE) is a newly recognized factor regulating cancer cell invasion and metastasis. This study investigated the expression of RAGE in gastric carcinomas and its association with invasion and metastasis. Of eight gastric cancer cell lines examined, seven constitutively expressed RAGE messenger ribonucleic acid (mRNA), MKN45 being the exception. RAGE protein expression of MKN28 cells treated with RAGE antisense S-oligodeoxynucleotide was nine times less than that of sense S-oligodeoxynucleotide-treated cells. Growth of cells under RAGE antisense S-oligodeoxynucleotide treatment was not different from that seen under sense S-oligodeoxynucleotide treatment in MKN28 (a cell line producing high levels of RAGE) and MKN45 (a non-RAGE-expressing cell line). RAGE antisense S-oligodeoxynucleotide treatment suppressed the invasive activity of RAGE-positive MKN28 cells, as estimated by in vitro invasion assay. The number of MKN28 cells invading the type IV collagen-coated membrane under RAGE antisense S-oligodeoxynucleotide treatment was significantly lower than under RAGE sense S-oligodeoxynucleotide treatment (p<0.0001). In contrast, antisense and sense S-oligodeoxynucleotide-treated RAGE-negative MKN45 cells showed no difference. A wound-healing assay showed that no RAGE antisense S-oligodeoxynucleotide-treated MKN28 cells migrated into the scraped area, whereas sense S-oligodeoxynucleotide-treated cells showed many budding nests in the scraped area. Immunohistochemistry of gastric carcinoma tissue showed that 62 (65%) of the 96 cases examined were RAGE-positive and that poorly differentiated adenocarcinomas preferentially expressed RAGE protein (38/42, 90%) (p<0.0001). Strong RAGE immunoreactivity was also correlated with depth of invasion and lymph node metastasis (p<0.0001). RAGE-positive cancer cells tended to be distributed at the invasive front of primary tumours and were detected in all metastatic foci in lymph nodes. In contrast, a major RAGE ligand, amphoterin, was expressed in 82 (85%) of the 96 cases, regardless of histological type and disease progression. RAGE expression appears to be closely associated with invasion and metastasis in gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression of receptors for advanced glycation end‐products (RAGE) is closely associated with the invasive and metastatic activity of gastric cancer

Kuniyasu

Oue

Wakikawa

et al. 2001

The Journal of Pathology

290

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“…As described earlier, all the eight gastric cancer cell lines expressed c‐met, a receptor for HGF/SF. Exogenous HGF/SF or fibroblast coculture induced scattering in TMK‐1 poorly‐differentiated adenocarcinoma cell line on 0.1% collagen gel, 58 while these treatments resulted in enhanced tubulogenesis in MKN‐28 well‐differentiated adenocarcinoma cell line in 0.1% collagen gel. 59 The expression of HGF/SF mRNA was not detected in these cell lines with the exception of HSC‐39.…”

Section: Growth Factors and Their Receptorsmentioning

confidence: 98%

“…Exogenous HGF/SF or fibroblast coculture induced scattering in TMK‐1 poorly‐differentiated adenocarcinoma cell line on 0.1% collagen gel, 58 while these treatments resulted in enhanced tubulogenesis in MKN‐28 well‐differentiated adenocarcinoma cell line in 0.1% collagen gel. 59 The expression of HGF/SF mRNA was not detected in these cell lines with the exception of HSC‐39. HSC‐39 expressed a HGF/SF transcript with abnormal size that was confirmed to be composed of a part of HGF/SF cDNA from exon 14 to exon 18, corresponding to the whole sequence of HGF/SF light chain.…”

Section: Growth Factors and Their Receptorsmentioning

confidence: 98%

Molecular characteristics of eight gastric cancer cell lines established in Japan

Yokozaki

2000

Pathology International

174

142

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Molecular characterization of eight gastric cancer cell lines established in Japan are summarized according to the genetic and epigenetic alterations and growth factor status. TMK-1 poorly differentiated adenocarcinoma cell line harbors mutant p53 tumor suppressor gene and rearrangement of p15MTS2. MKN-1 adenosquamous carcinoma line with mutant p53 reveals silencing of E-cadherin by promoter CpG hypermethylation. MKN-7 well-differentiated adenocarcinoma cell line has amplification of c-erbB2 oncogene and cyclin E gene. MKN-28 well-differentiated adenocarcinoma cell line reveals mutations in p53 and APC tumor suppressor genes and silencing of CD44. The MKN-45 poorly differentiated adenocarcinoma cell line with wild-type p53 is characterized by homozygous deletion of p16CDKN2/MTS1/INK4A and p15MTS2, amplification of c-met oncogene and promoter mutation of E-cadherin. MKN-74 derived from moderately differentiated tubular adenocarcinoma has wild-type p53. KATO-III signet ring cell carcinoma line has genomic deletion of p53, amplification of K-sam and c-met oncogene and mutation of E-cadherin. HSC-39 signet ring cell carcinoma cell line harboring p53 missense mutation has homozygous deletion of p16CDKN2/MTS1/INK4A and p15MTS2, amplifications of c-myc, c-met, K-sam and CD44 gene and mutation in beta-catenin gene.

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“…As a first‐step of the analysis of CSIs, a co‐culture system separating cancer and stromal cells with 0.1% collagen gel was developed. TMK‐1 cells, a line of poorly differentiated gastric cancer (GC) cells, showed marked scattering on collagen gel when co‐cultured with stomach derived fibroblasts, whereas well‐differentiated type MKN‐28 cells exhibited tubular formation within the collagen gel by fibroblast co‐culture via a hepatocellular growth factor/MET paracrine loop …”

Section: Interaction Between Cancer Cells and Fibroblasts In The Morpmentioning

confidence: 99%

Cancer as a tissue: The significance of cancer‐stromal interactions in the development, morphogenesis and progression of human upper digestive tract cancer

Yokozaki

Koma

Shigeoka

et al. 2018

Pathology International

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We review the significance of cancer-stromal interactions (CSIs) in the development, morphogenesis and progression of human gastric and esophageal cancer based on the data obtained from co-culture experiments. Orthotopic fibroblasts in the gastric cancer stroma not only promoted their growth by cancer cells but were also responsible for the mobility, morphogenesis and epithelial-to-mesenchymal transition (EMT) of the cancer cells through CSI. Bone marrow-derived mesenchymal stem cells could be part of the origin of cancer-associated fibroblasts (CAFs) of the gastric cancer providing an advantageous microenvironment for the restoration of cancer stem cells with the induction of the EMT. Tumor-associated macrophages (TAMs) may differentiate from bone marrow-derived monocytes/macrophages within the tumor microenvironment of esophageal cancer and participate in the growth and the progression of esophageal squamous cell carcinomas (ESCCs). Macrophages infiltrated into the intraepithelial neoplastic lesions of the esophagus may function as a biological promoter by promoting the growth and motility of squamous epithelia. Tumor cells build up "cancer as a tissue" by taking advantage of the existing network of growth factors, cytokines and chemokines through the interactions of TAMs, CAFs and cancer cells themselves.

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Biologic Effect of Human Hepatocyte Growth-Factor on Human Gastric-Carcinoma Cell-Lines

Cited by 5 publications

References 0 publications

Expression of receptors for advanced glycation end‐products (RAGE) is closely associated with the invasive and metastatic activity of gastric cancer

Expression of receptors for advanced glycation end‐products (RAGE) is closely associated with the invasive and metastatic activity of gastric cancer

Molecular characteristics of eight gastric cancer cell lines established in Japan

Cancer as a tissue: The significance of cancer‐stromal interactions in the development, morphogenesis and progression of human upper digestive tract cancer

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