Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin A level and the cytosol-binding proteins specific for vitamin A ere studied in human tumor and its surrounding tissue. The tissues examined were 10 hepatocellular carcinomas which were surgically removed, 4 other malignant tumors (2 metastatic liver cancer and one each of gastric cancer and glioma), and 3 human fetal livers. Compared with surrounding tissues, considerable decrease of vitamin A content was observed in the hepatocellular carcinoma suggesting local deficient state of the vitamin. In addition to cellular retinol-binding protein (CRBP) and retinoic acid-binding protein (CRABP), a new molecular species having affinity for both retinol and retinoic acid was detected in the cytosols obtained from hepatocellular carcinoma as well as glioma by means of gel filtration on Sephadex G-75. With regard to ligand specificity, the protein was found to be similar to cellular retinol-binding protein, F-type or CRBP(F) which was originally recognized in the fish eye cytosol. Since the protein was also demonstrated in human fetal liver, CRBP(F) is considered to be an oncofetal protein in nature. The present study further revealed that CRBP(F) was detected in 80% of hepatocellular carcinoma (whereas plasma alpha-fetoprotein was significantly elevated only in 50%), and hepatocellular carcinoma contained CRBP(F) in a larger amount than CRABP.
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PMID:Demonstration of a novel cellular retinol-binding protein, F-type, in hepatocellular carcinoma. 8 58

The growth of a human gastric adenocarcinoma cell line, MKN-45, was inhibited and the amount of carcinoembryonic antigen (CEA) in both the culture medium and the cell extract was increased in the presence of retinoic acid at a concentration of 75 (1.5x)-125 microM (1.9x), which did not substantially affect cell survival. Treatment using a combination of retinoic acid (125 microM) and low-temperature hyperthermia (40 degrees C, 30 min) was more effective in increasing CEA compared with retinoic acid alone (extracellular 1.9-2.4x, intracellular 1.5-1.9x). The inhibition of cell growth was reversed after the retinoic acid was removed from the medium. Cells treated with both retinoic acid and (low-temperature) hyperthermia, however, could be induced to release a significant amount of CEA at about 48 h after retinoic acid removal. The induced CEA increase in the cells, but not in the medium, was suppressed by actinomycin D (1 ng/ml) or cyclohexamide (0.2 microgram/ml). These results suggest that retinoic acid, used alone or in combination with hyperthermia, enhances the production and release of CEA in human gastric cancer cells.
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PMID:Increase in carcinoembryonic antigen release from cancer cells by combined treatment with retinoic acid and low-temperature hyperthermia. 239 26

The human gastric cancer cell lines, MKN1 and SCH, were biochemically and biologically characterized according to the monophenotypic expression of placental alkaline phosphatase (PLAP)-like enzymes. The MKN1 cell line, derived from adenosquamous carcinoma, showed the same enzyme properties as the Regan isoenzyme, whereas the SCH cell line, derived from primary gastric choriocarcinoma, had properties identical with the Nagao isoenzyme. Regan isoenzyme activity expressed by MKN1 cells was stimulated by glucocorticoid and suppressed by retinoic acid. Both agents had no significant effect on SCH cells. On the other hand, Nagao isoenzyme activity expressed by SCH cells was stimulated by sodium butyrate, which had no stimulatory effect on MKN1 cells. Moreover, the PLAP-like activity of MKN1 cells showed no observable relationship to human chorionic gonadotropin (hCG)-producibility. Whereas expression of the Nagao isoenzyme by the SCH cell line is presumably a result of functional differentiation in the trophoblastic direction, that of the Regan isoenzyme by the MKN1 cell line is probably not. Perhaps the Regan isoenzyme is related to carcinogenesis.
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PMID:Placental alkaline phosphatase-like isoenzymes produced by human gastric cancer cells. 268 48

We have extended our recent observation that human gastric cancer cells (MKN-45) synthesize and secrete an hEGF-like immunoreactive factor (designated as EGF-LI) by characterization of EGF-LI produced by five human gastric cancer cell lines in culture. Two cell lines (MKN-45 and KATO-III) derived from poorly differentiated adenocarcinoma synthesized and secreted a much larger amount of EGF-LI than three cell lines (MKN-1, MKN-28, and MKN-74) derived from well-differentiated adenocarcinoma. Treatment of MKN-45 cells by retinoic acid reduced significantly synthesis and secretion of EGF-LI, suggesting that production of EGF-LI is dependent on differentiational state of gastric cancer cells.
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PMID:Production of an hEGF-like immunoreactive factor by human gastric cancer cells depends on differentiational state of the cells. 330 Jun 42

Retinoic acid has been recognised as a pivotal compound in cell differentiation, proliferation and malignant transformation. We investigated the effects of all-trans-retinoic acid on cell growth and the expression of retinoid nuclear receptor mRNAs in gastric cancer cells in vitro. Cell growth was quantified by measuring total cellular DNA. The growth of two of the five gastric cancer cell lines tested (SC-M1 and TSGH9201) was inhibited by all-trans-retinoic acid at concentrations ranging from 1 x 10(-8) M to 1 x 10(-6) M. Growth inhibition was associated with G0/G1 phase arrest as determined by flow cytometric analysis. Northern blot analysis showed that all five cell lines expressed mRNA for retinoic acid receptors alpha and retinoic x receptor alpha and beta. Retinoic acid receptor beta mRNA was only expressed in TSGH9201 and TMK-1 gastric cancer cell lines. Two RAR gamma mRNA transcripts (3.2 and 3.0 kb) were detected in SC-M1 and TSGH9201 cells. RA-resistant cells had markedly decreased levels of the 3.2 kb RAR gamma transcript. All-trans-retinoic acid had a cytostatic effect on the growth of some gastric cancer cells, which may be associated with the expression of retinoic acid receptors.
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PMID:Growth regulation by all-trans-retinoic acid and retinoic acid receptor messenger ribonucleic acids expression in gastric cancer cells. 771 31

The growth rate and weight of transplanted tumor of SGC7901 gastric cancer cell line, treated with 10 mumol/L retinoic acid (RA) in nude mice, were significantly reduced in comparison with those of control cells. The morphology of RA-treated cells was changed from ellipse shape with meandering margin of a large nucleus to shuttle shape with smooth margin of a small nucleus. With flow cytometry, it was found that G/O Phase markedly increased after the RA treatment, whereas S and G2 + M phase decreased. Especially the S phase fraction was lower than that of control cells. The above results indicated that RA could reverse biological and morphological phenotypes of the human gastric cancer cells in vitro and could induce differentiation of gastric cancer cells to a certain extent.
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PMID:[Induction of differentiation of human gastric cancer cell line by retinoic acid]. 803 40

The aim of this study was to survey the expression of an embryonic cytokine gene, MK, in the normal organs and neoplastic tissues of adults. Northern analysis showed that MK mRNA was exclusively expressed in the kidney among murine organs including thymus, lung, heart, spleen, liver, and kidney. In situ hybridization analysis revealed that MK expression was localized in the proximal tubules and metaplastic Bowman's epithelium, but not in other nephron segments such as glomeruli, loop of Henle, distal tubules, and collecting ducts. To investigate whether MK expression is a marker of tubular cell lineage, several cell lines originating from renal tubules were tested. No expression of MK was detected in PtK1 and LLC-PK1 cells derived from marsupial and porcine proximal tubules or in MDBK and MDCK cells from bovine and canine distal/collecting tubules. Unexpectedly, the MK gene was expressed in a human renal cell carcinoma line, VMRC-RCW, and the expression was up-regulated in the presence of retinoic acid. To elucidate the involvement of MK in the development of tumors, we further examined its expression in a variety of human neoplastic cell lines: YMB-1-C (breast cancer), EBC-1 (lung squamous cell carcinoma), RERF-LC-OK (lung adenocarcinoma), SBC-3 (lung small cell carcinoma), HSC-2 (mouth squamous cell carcinoma), NUGC-2 (gastric cancer), COLO201 (colon cancer), HepG2 (hepatoma), MIA PaCa-2 (pancreatic cancer), MCAS (ovarian cancer), HeLa (cervical cancer), BeWo (chorionic carcinoma), ITO-II (testicular tumor), T24 (urinary bladder tumor), and G-401 (Wilms' tumor). Strong signals were detected in COLO201, HepG2, ITO-II, T24, G-401, and weaker but distinct signals were detected in YMB-1-C, HSC-2, and MCAS cells. The MK gene was, therefore, widely expressed in neoplastic cells originating from genital organs, intestinal tract, liver, mammary gland, and urinary tract, and the expression was not restricted to adenocarcinomas, but was also observed in other types of tumor cells. These findings suggest that a retinoic acid responsive gene, MK, may play a role in the pathophysiology of renal proximal tubules and tumorigenesis in many types of neoplasms.
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PMID:A retinoid responsive cytokine gene, MK, is preferentially expressed in the proximal tubules of the kidney and human tumor cell lines. 843 39

We found that vitamin D3 up-regulates the expression of cytidine deaminase (CDD) gene in some human solid tumor cell lines as well as the monocytic leukemia cell lines. Two kinds of full length CDD cDNA were identified from human placenta: one has glutamine and the other one has lysine at codon 27. The expression was tested in various normal tissues and the cancer cell lines. Northern blot analysis demonstrated high levels of CDD mRNA in leukocytes and moderate levels in liver, kidney, placenta, spleen and lung. Expression of CDD in 20 human cancer cell lines was highly variable and not related to its expression in normal tissues. Treatment of the cell lines with 1 alpha,25-dihydroxyvitamin D3 resulted in up-regulation of CDD expression in some lines but not others. Three of five gastric carcinoma cell lines and five of eight colorectal cancer lines had increased levels of CDD mRNA following 24 h treatment with vitamin D3. Increased mRNA was detected in gastric cancer MKN 45 cells after 3 h of treatment with vitamin D3 and increased enzyme activity was measured after 24 to 48 h. But no combined effect of calcitriol with 9-cis retinoic acid was found. Our results demonstrate that CDD can be up-regulated by vitamin D3 in some solid tumor cell lines.
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PMID:Expression of cytidine deaminase in human solid tumors and its regulation by 1 alpha,25-dihydroxyvitamin D3. 867 45

Retinoids are differentiating agents that have been used successfully for the treatment of acute promyelocytic leukemia. When combined with interferons, they are active in preventing second malignancies in patients with head and neck cancer. Our previous studies have demonstrated cytostatic effects of alltrans-retinoic acid (tRA) on SC-M1 gastric cancer cells in vitro. The activity of tRA and 13-cis-retinoic acid (cRA) on SC-M1 cells was compared both in vitro and in vivo in this study. Measurement of total cellular DNA was used to determine cell growth in vitro. The effect of retinoic acid on tumor growth was evaluated by implanting sustained release tRA or cRA pellets into athymic nude mice. The results showed that tRA was more potent than cRA in suppressing the growth of SC-M1 gastric cancer cells in vitro. Both tRA and cRA were effective in suppressing the growth of SC-M1 tumors in athymic nude mice. No change in the differentiation status and cell cycle phase distribution in excised tumors was observed. Side effects such as bone fractures and weight loss were observed in mice of both treatment groups. The results suggest that retinoic acid may provide therapeutic advantages for the treatment of gastric cancer.
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PMID:In vitro and in vivo growth inhibition of SC-M1 gastric cancer cells by retinoic acid. 869 40

All-trans retinoic acid (RA) was previously shown to regulate the growth of gastric cancer cells derived from the cell line SC-M1. This study was designed to investigate the effect of RA on the sensitivity of SC-M1 cells to lymphokine-activated killer (LAK) activity. RA at the concentration range of 0.001-10 microM was shown to induce SC-M1 cells to exhibit resistance to LAK activity in a dose-dependent manner. A kinetics study indicated that a significantly increased resistance was detected after 2 days of co-culturing SC-M1 cells with RA and reached a maximum after 6 days of culture. Similar results were obtained from two other cancer cell lines: promyelocytic leukaemia HL-60 and hepatic cancer Hep 3B. A binding assay demonstrated that the binding efficacy between target SC-M1 cells and effector LAK cells was not altered by RA. Flow cytometric analyses revealed that RA exhibited no effect on the expression of cell surface molecules, including HLA class I and class II antigens, intercellular adhesion molecule-1 and -2, and lymphocyte function antigen-3. Cell cycle analysis revealed that culture of SC-M1 cells with RA resulted in an increase in G0/G1 phase and a decrease in S phase, accompanied by a decrease in cyclin A and cyclin B1 mRNA as determined by Northern blot analysis. Additionally, RA was shown to enhance the expression of retinoic acid receptor alpha (RAR alpha) in SC-M1 cells, and to have no effect on the expression of RARbeta or RARgamma. Taken together, these results indicate that RA can significantly increase gastric cancer cells SC-M1 to resist LAK cytotoxicity by means of a cytostatic effect through a mechanism relating to cell cycle regulation. The prevailing ideas, such as a decrease in effector to target cell binding, a reduced MHC class I antigen expression or an altered RARbeta expression, are not involved.
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PMID:All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity. 915 47


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