Colon cancer cells that are not growth inhibited by TGF-beta lack functional type I and type II TGF-beta receptors
The authors determined the molecular mechanisms for the failure of transforming growth factor-beta (TGF-beta) to inhibit the growth of SW1116 and SW48 colon cancer cell lines. Transforming growth factor-beta is a bifunctional regulator of cell growth that typically stimulates proliferation of mesenc...
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| Veröffentlicht in: | Annals of surgery 1995-06, Vol.221 (6), p.767-777 |
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| creator | MacKay, S L Yaswen, L R Tarnuzzer, R W Moldawer, L L Bland, K I Copeland, 3rd, E M Schultz, G S |
| description | The authors determined the molecular mechanisms for the failure of transforming growth factor-beta (TGF-beta) to inhibit the growth of SW1116 and SW48 colon cancer cell lines.
Transforming growth factor-beta is a bifunctional regulator of cell growth that typically stimulates proliferation of mesenchymal cells, but inhibits proliferation of normal epithelial cells. In the colon, TGF-beta appears to arrest proliferation of enterocytes as they leave the intestinal crypt and move to the villus tip. Transforming growth factor-beta actions are mediated by binding to heteromeric complexes of type I and type II TGF-beta receptors. Loss of TGF-beta responsiveness may contribute to uncontrolled cell growth and cancer.
The effects of TGF-beta 1 on DNA synthesis were measured by incorporation of tritiated thymidine into DNA of cultures of moderately differentiated adenocarcinoma (SW48) and poorly differentiated adenocarcinoma (SW1116) colon cell lines and a mink lung epithelial cell line (CCL-64). The effects of TGF-beta on the expression of c-myc, TGF-alpha, and TGF-beta in SW48 cells, SW1116 cells, and CCL-64 cells (c-myc only) were measured by Northern blot analysis. Expression of TGF-beta receptors in the cell lines was measured using competitive binding assays, receptor affinity labelling techniques, and reverse transcriptase-polymerase chain reaction.
Incubation with TGF-beta 1 (50 ng/mL) did not decrease serum-stimulated uptake of [3H]-thymidine into actively growing cultures of SW48 or SW1116 cells, but suppressed DNA synthesis of actively growing CCL-64 cells by 90%. Similarly, incubation with TGF-beta 1 (12 ng/mL) for 4 hours did not substantially alter the mRNA levels of c-myc, TGF-alpha, and TGF-beta 1 in either colon tumor cell line, although levels of c-myc mRNA in CCL-64 cells were reduced by TGF-beta 1 treatment. Competitive displacement of [125I]-TGF-beta 1 binding detected high levels (16,500 TGF-beta receptors per cell) of specific, high-affinity (200 pmol/L half-displacement) TGF-beta receptors on CCL-64 cells. In marked contrast, very low levels of TGF-beta 1 binding to SW1116 cells (250 receptors per cell) and SW48 cells (260 receptors per cell) were detected. Autoradiograms of CCL-64 cells affinity labelled with [125I]TGF-beta 1 revealed the presence of type I, type II, and type III TGF-beta receptors. No TGF-beta receptors were identified on SW1116 cells, and only very low levels of the nonsignaling type III TGF-beta receptors were detected on |
| doi_str_mv | 10.1097/00000658-199506000-00015 |
| format | Article |
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Transforming growth factor-beta is a bifunctional regulator of cell growth that typically stimulates proliferation of mesenchymal cells, but inhibits proliferation of normal epithelial cells. In the colon, TGF-beta appears to arrest proliferation of enterocytes as they leave the intestinal crypt and move to the villus tip. Transforming growth factor-beta actions are mediated by binding to heteromeric complexes of type I and type II TGF-beta receptors. Loss of TGF-beta responsiveness may contribute to uncontrolled cell growth and cancer.
The effects of TGF-beta 1 on DNA synthesis were measured by incorporation of tritiated thymidine into DNA of cultures of moderately differentiated adenocarcinoma (SW48) and poorly differentiated adenocarcinoma (SW1116) colon cell lines and a mink lung epithelial cell line (CCL-64). The effects of TGF-beta on the expression of c-myc, TGF-alpha, and TGF-beta in SW48 cells, SW1116 cells, and CCL-64 cells (c-myc only) were measured by Northern blot analysis. Expression of TGF-beta receptors in the cell lines was measured using competitive binding assays, receptor affinity labelling techniques, and reverse transcriptase-polymerase chain reaction.
Incubation with TGF-beta 1 (50 ng/mL) did not decrease serum-stimulated uptake of [3H]-thymidine into actively growing cultures of SW48 or SW1116 cells, but suppressed DNA synthesis of actively growing CCL-64 cells by 90%. Similarly, incubation with TGF-beta 1 (12 ng/mL) for 4 hours did not substantially alter the mRNA levels of c-myc, TGF-alpha, and TGF-beta 1 in either colon tumor cell line, although levels of c-myc mRNA in CCL-64 cells were reduced by TGF-beta 1 treatment. Competitive displacement of [125I]-TGF-beta 1 binding detected high levels (16,500 TGF-beta receptors per cell) of specific, high-affinity (200 pmol/L half-displacement) TGF-beta receptors on CCL-64 cells. In marked contrast, very low levels of TGF-beta 1 binding to SW1116 cells (250 receptors per cell) and SW48 cells (260 receptors per cell) were detected. Autoradiograms of CCL-64 cells affinity labelled with [125I]TGF-beta 1 revealed the presence of type I, type II, and type III TGF-beta receptors. No TGF-beta receptors were identified on SW1116 cells, and only very low levels of the nonsignaling type III TGF-beta receptors were detected on SW48 cells. Reverse transcriptase-polymerase chain reaction amplification detected mRNAs for type I, type II, and type III TGF-beta receptors in CCL-64 cells. SW48 cells, and SW1116 cells.
These results suggest that the lack of growth inhibition by TGF-beta in SW48 and SW1116 colon cancer cells may be caused by a lack of expression of functional TGF-beta receptors.</description><identifier>ISSN: 0003-4932</identifier><identifier>EISSN: 1528-1140</identifier><identifier>DOI: 10.1097/00000658-199506000-00015</identifier><identifier>PMID: 7794080</identifier><language>eng</language><publisher>United States</publisher><subject>Activin Receptors, Type I ; Base Sequence ; Cell Division - drug effects ; Colonic Neoplasms - pathology ; DNA, Neoplasm - biosynthesis ; Epithelium - chemistry ; Genes, myc - genetics ; Humans ; Molecular Sequence Data ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases ; Proteoglycans - genetics ; Receptor, Transforming Growth Factor-beta Type I ; Receptor, Transforming Growth Factor-beta Type II ; Receptors, Transforming Growth Factor beta - genetics ; Receptors, Transforming Growth Factor beta - physiology ; RNA, Messenger - analysis ; Transforming Growth Factor alpha - genetics ; Transforming Growth Factor beta - pharmacology ; Tumor Cells, Cultured</subject><ispartof>Annals of surgery, 1995-06, Vol.221 (6), p.767-777</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-1077fb5f1af3134706c85ac42b1877fad6c7c82b7c3b9416b04209d7a04dfc983</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1234710/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1234710/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7794080$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MacKay, S L</creatorcontrib><creatorcontrib>Yaswen, L R</creatorcontrib><creatorcontrib>Tarnuzzer, R W</creatorcontrib><creatorcontrib>Moldawer, L L</creatorcontrib><creatorcontrib>Bland, K I</creatorcontrib><creatorcontrib>Copeland, 3rd, E M</creatorcontrib><creatorcontrib>Schultz, G S</creatorcontrib><title>Colon cancer cells that are not growth inhibited by TGF-beta lack functional type I and type II TGF-beta receptors</title><title>Annals of surgery</title><addtitle>Ann Surg</addtitle><description>The authors determined the molecular mechanisms for the failure of transforming growth factor-beta (TGF-beta) to inhibit the growth of SW1116 and SW48 colon cancer cell lines.
Transforming growth factor-beta is a bifunctional regulator of cell growth that typically stimulates proliferation of mesenchymal cells, but inhibits proliferation of normal epithelial cells. In the colon, TGF-beta appears to arrest proliferation of enterocytes as they leave the intestinal crypt and move to the villus tip. Transforming growth factor-beta actions are mediated by binding to heteromeric complexes of type I and type II TGF-beta receptors. Loss of TGF-beta responsiveness may contribute to uncontrolled cell growth and cancer.
The effects of TGF-beta 1 on DNA synthesis were measured by incorporation of tritiated thymidine into DNA of cultures of moderately differentiated adenocarcinoma (SW48) and poorly differentiated adenocarcinoma (SW1116) colon cell lines and a mink lung epithelial cell line (CCL-64). The effects of TGF-beta on the expression of c-myc, TGF-alpha, and TGF-beta in SW48 cells, SW1116 cells, and CCL-64 cells (c-myc only) were measured by Northern blot analysis. Expression of TGF-beta receptors in the cell lines was measured using competitive binding assays, receptor affinity labelling techniques, and reverse transcriptase-polymerase chain reaction.
Incubation with TGF-beta 1 (50 ng/mL) did not decrease serum-stimulated uptake of [3H]-thymidine into actively growing cultures of SW48 or SW1116 cells, but suppressed DNA synthesis of actively growing CCL-64 cells by 90%. Similarly, incubation with TGF-beta 1 (12 ng/mL) for 4 hours did not substantially alter the mRNA levels of c-myc, TGF-alpha, and TGF-beta 1 in either colon tumor cell line, although levels of c-myc mRNA in CCL-64 cells were reduced by TGF-beta 1 treatment. Competitive displacement of [125I]-TGF-beta 1 binding detected high levels (16,500 TGF-beta receptors per cell) of specific, high-affinity (200 pmol/L half-displacement) TGF-beta receptors on CCL-64 cells. In marked contrast, very low levels of TGF-beta 1 binding to SW1116 cells (250 receptors per cell) and SW48 cells (260 receptors per cell) were detected. Autoradiograms of CCL-64 cells affinity labelled with [125I]TGF-beta 1 revealed the presence of type I, type II, and type III TGF-beta receptors. No TGF-beta receptors were identified on SW1116 cells, and only very low levels of the nonsignaling type III TGF-beta receptors were detected on SW48 cells. Reverse transcriptase-polymerase chain reaction amplification detected mRNAs for type I, type II, and type III TGF-beta receptors in CCL-64 cells. SW48 cells, and SW1116 cells.
These results suggest that the lack of growth inhibition by TGF-beta in SW48 and SW1116 colon cancer cells may be caused by a lack of expression of functional TGF-beta receptors.</description><subject>Activin Receptors, Type I</subject><subject>Base Sequence</subject><subject>Cell Division - drug effects</subject><subject>Colonic Neoplasms - pathology</subject><subject>DNA, Neoplasm - biosynthesis</subject><subject>Epithelium - chemistry</subject><subject>Genes, myc - genetics</subject><subject>Humans</subject><subject>Molecular Sequence Data</subject><subject>Polymerase Chain Reaction</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Proteoglycans - genetics</subject><subject>Receptor, Transforming Growth Factor-beta Type I</subject><subject>Receptor, Transforming Growth Factor-beta Type II</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Receptors, Transforming Growth Factor beta - physiology</subject><subject>RNA, Messenger - analysis</subject><subject>Transforming Growth Factor alpha - genetics</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Tumor Cells, Cultured</subject><issn>0003-4932</issn><issn>1528-1140</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkdFOwyAUhonRzDl9BBOuvKtCS0u5MTGLm0uWeDOvCVC6VjuYQDV7e5mrU0kIh3P-8x_CBwDE6BYjRu_QfhV5mWDGclTESxI3zk_AGOdpTGOCTsE45rKEsCw9Bxfev0YFKREdgRGljKASjYGb2s4aqIRR2kGlu87D0IgAhdPQ2ADXzn6GBramaWUbdAXlDq7ms0TqIGAn1Buse6NCa43oYNhtNVxAYaohXPxqnVZ6G6zzl-CsFp3XV8M5AS-zx9X0KVk-zxfTh2WiCM5DghGltcxrLOoMZ4SiQpW5UCSVuIwVURWKqjKVVGWSEVxIRFLEKioQqWrFymwC7g--215udKW0CU50fOvajXA7bkXL_1dM2_C1_eA4jeMwigY3g4Gz7732gW9av_8iYbTtPac0yymhLArLg1A5673T9XEIRnzPi__w4kde_JtXbL3--8hj4wAo-wKQx5Fi</recordid><startdate>19950601</startdate><enddate>19950601</enddate><creator>MacKay, S L</creator><creator>Yaswen, L R</creator><creator>Tarnuzzer, R W</creator><creator>Moldawer, L L</creator><creator>Bland, K I</creator><creator>Copeland, 3rd, E M</creator><creator>Schultz, G S</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19950601</creationdate><title>Colon cancer cells that are not growth inhibited by TGF-beta lack functional type I and type II TGF-beta receptors</title><author>MacKay, S L ; Yaswen, L R ; Tarnuzzer, R W ; Moldawer, L L ; Bland, K I ; Copeland, 3rd, E M ; Schultz, G S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-1077fb5f1af3134706c85ac42b1877fad6c7c82b7c3b9416b04209d7a04dfc983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Activin Receptors, Type I</topic><topic>Base Sequence</topic><topic>Cell Division - drug effects</topic><topic>Colonic Neoplasms - pathology</topic><topic>DNA, Neoplasm - biosynthesis</topic><topic>Epithelium - chemistry</topic><topic>Genes, myc - genetics</topic><topic>Humans</topic><topic>Molecular Sequence Data</topic><topic>Polymerase Chain Reaction</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Proteoglycans - genetics</topic><topic>Receptor, Transforming Growth Factor-beta Type I</topic><topic>Receptor, Transforming Growth Factor-beta Type II</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Receptors, Transforming Growth Factor beta - physiology</topic><topic>RNA, Messenger - analysis</topic><topic>Transforming Growth Factor alpha - genetics</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MacKay, S L</creatorcontrib><creatorcontrib>Yaswen, L R</creatorcontrib><creatorcontrib>Tarnuzzer, R W</creatorcontrib><creatorcontrib>Moldawer, L L</creatorcontrib><creatorcontrib>Bland, K I</creatorcontrib><creatorcontrib>Copeland, 3rd, E M</creatorcontrib><creatorcontrib>Schultz, G S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MacKay, S L</au><au>Yaswen, L R</au><au>Tarnuzzer, R W</au><au>Moldawer, L L</au><au>Bland, K I</au><au>Copeland, 3rd, E M</au><au>Schultz, G S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Colon cancer cells that are not growth inhibited by TGF-beta lack functional type I and type II TGF-beta receptors</atitle><jtitle>Annals of surgery</jtitle><addtitle>Ann Surg</addtitle><date>1995-06-01</date><risdate>1995</risdate><volume>221</volume><issue>6</issue><spage>767</spage><epage>777</epage><pages>767-777</pages><issn>0003-4932</issn><eissn>1528-1140</eissn><abstract>The authors determined the molecular mechanisms for the failure of transforming growth factor-beta (TGF-beta) to inhibit the growth of SW1116 and SW48 colon cancer cell lines.
Transforming growth factor-beta is a bifunctional regulator of cell growth that typically stimulates proliferation of mesenchymal cells, but inhibits proliferation of normal epithelial cells. In the colon, TGF-beta appears to arrest proliferation of enterocytes as they leave the intestinal crypt and move to the villus tip. Transforming growth factor-beta actions are mediated by binding to heteromeric complexes of type I and type II TGF-beta receptors. Loss of TGF-beta responsiveness may contribute to uncontrolled cell growth and cancer.
The effects of TGF-beta 1 on DNA synthesis were measured by incorporation of tritiated thymidine into DNA of cultures of moderately differentiated adenocarcinoma (SW48) and poorly differentiated adenocarcinoma (SW1116) colon cell lines and a mink lung epithelial cell line (CCL-64). The effects of TGF-beta on the expression of c-myc, TGF-alpha, and TGF-beta in SW48 cells, SW1116 cells, and CCL-64 cells (c-myc only) were measured by Northern blot analysis. Expression of TGF-beta receptors in the cell lines was measured using competitive binding assays, receptor affinity labelling techniques, and reverse transcriptase-polymerase chain reaction.
Incubation with TGF-beta 1 (50 ng/mL) did not decrease serum-stimulated uptake of [3H]-thymidine into actively growing cultures of SW48 or SW1116 cells, but suppressed DNA synthesis of actively growing CCL-64 cells by 90%. Similarly, incubation with TGF-beta 1 (12 ng/mL) for 4 hours did not substantially alter the mRNA levels of c-myc, TGF-alpha, and TGF-beta 1 in either colon tumor cell line, although levels of c-myc mRNA in CCL-64 cells were reduced by TGF-beta 1 treatment. Competitive displacement of [125I]-TGF-beta 1 binding detected high levels (16,500 TGF-beta receptors per cell) of specific, high-affinity (200 pmol/L half-displacement) TGF-beta receptors on CCL-64 cells. In marked contrast, very low levels of TGF-beta 1 binding to SW1116 cells (250 receptors per cell) and SW48 cells (260 receptors per cell) were detected. Autoradiograms of CCL-64 cells affinity labelled with [125I]TGF-beta 1 revealed the presence of type I, type II, and type III TGF-beta receptors. No TGF-beta receptors were identified on SW1116 cells, and only very low levels of the nonsignaling type III TGF-beta receptors were detected on SW48 cells. Reverse transcriptase-polymerase chain reaction amplification detected mRNAs for type I, type II, and type III TGF-beta receptors in CCL-64 cells. SW48 cells, and SW1116 cells.
These results suggest that the lack of growth inhibition by TGF-beta in SW48 and SW1116 colon cancer cells may be caused by a lack of expression of functional TGF-beta receptors.</abstract><cop>United States</cop><pmid>7794080</pmid><doi>10.1097/00000658-199506000-00015</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Annals of surgery, 1995-06, Vol.221 (6), p.767-777 |
| issn | 0003-4932 1528-1140 |
| language | eng |
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| source | MEDLINE; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Activin Receptors, Type I Base Sequence Cell Division - drug effects Colonic Neoplasms - pathology DNA, Neoplasm - biosynthesis Epithelium - chemistry Genes, myc - genetics Humans Molecular Sequence Data Polymerase Chain Reaction Protein-Serine-Threonine Kinases Proteoglycans - genetics Receptor, Transforming Growth Factor-beta Type I Receptor, Transforming Growth Factor-beta Type II Receptors, Transforming Growth Factor beta - genetics Receptors, Transforming Growth Factor beta - physiology RNA, Messenger - analysis Transforming Growth Factor alpha - genetics Transforming Growth Factor beta - pharmacology Tumor Cells, Cultured |
| title | Colon cancer cells that are not growth inhibited by TGF-beta lack functional type I and type II TGF-beta receptors |
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