<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kennedy A</submitter><funding>NIBIB NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>27-35</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2597700</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>124(1)</volume><pubmed_abstract>Tumor cells do not constitutively exhibit invasive activity, but rather, can be transiently induced to adhere and form lesions. We report here that the expression of seprase, a dominant EDTA-resistant gelatinase in malignant tumors, is dependent on tumor cell exposure to type I collagen gel (TICg). The induced seprase expression of ovarian tumor cells influences their collagen contraction and invasion capability. Importantly, tumor cells with reduced seprase expression, due to manipulation by RNA interference, showed a reduction of TICg contraction in the gel contractility assay, inhibition of tumor cell invasion through TICg as shown by a transwell migration assay and inhibition of peritoneal membrane tumor lesion in a mouse model. In addition, mAb C27, an antibody against beta1 integrin,</pubmed_abstract><journal>International journal of cancer</journal><pubmed_title>Elevation of seprase expression and promotion of an invasive phenotype by collagenous matrices in ovarian tumor cells.</pubmed_title><pmcid>PMC2597700</pmcid><funding_grant_id>M01 RR010710-070061</funding_grant_id><funding_grant_id>R01 CA039077-20</funding_grant_id><funding_grant_id>R41 CA103467-01</funding_grant_id><funding_grant_id>R01 CA039077-21</funding_grant_id><funding_grant_id>M01 RR010710</funding_grant_id><funding_grant_id>R01 CA039077-22</funding_grant_id><funding_grant_id>R01 CA039077-23</funding_grant_id><funding_grant_id>R01CA0039077</funding_grant_id><funding_grant_id>R01 EB002065</funding_grant_id><funding_grant_id>R01 EB002065-18</funding_grant_id><funding_grant_id>R01 EB002065-17</funding_grant_id><funding_grant_id>M01 RR010710-11</funding_grant_id><funding_grant_id>R01 EB002065-19</funding_grant_id><funding_grant_id>R01 EB002065-21</funding_grant_id><funding_grant_id>R01EB002065</funding_grant_id><funding_grant_id>R01 EB002065-20</funding_grant_id><funding_grant_id>R01 CA039077</funding_grant_id><pubmed_authors>Chen WT</pubmed_authors><pubmed_authors>Kennedy A</pubmed_authors><pubmed_authors>Dong H</pubmed_authors><pubmed_authors>Chen D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Elevation of seprase expression and promotion of an invasive phenotype by collagenous matrices in ovarian tumor cells.</name><description>Tumor cells do not constitutively exhibit invasive activity, but rather, can be transiently induced to adhere and form lesions. We report here that the expression of seprase, a dominant EDTA-resistant gelatinase in malignant tumors, is dependent on tumor cell exposure to type I collagen gel (TICg). The induced seprase expression of ovarian tumor cells influences their collagen contraction and invasion capability. Importantly, tumor cells with reduced seprase expression, due to manipulation by RNA interference, showed a reduction of TICg contraction in the gel contractility assay, inhibition of tumor cell invasion through TICg as shown by a transwell migration assay and inhibition of peritoneal membrane tumor lesion in a mouse model. In addition, mAb C27, an antibody against beta1 integrin,</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Jan</publication><modification>2025-04-21T21:01:21.058Z</modification><creation>2019-06-06T20:40:04Z</creation></dates><accession>S-EPMC2597700</accession><cross_references><pubmed>18823010</pubmed><doi>10.1002/ijc.23871</doi></cross_references></HashMap>