<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Su WP</submitter><funding>Ministry of Science and Technology, Taiwan</funding><funding>National Health Research Institutes</funding><pagination>E2189</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7464583</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(8)</volume><pubmed_abstract>Synthetic Zfra4-10 and WWOX7-21 peptides strongly suppress cancer growth in vivo. Hypothetically, Zfra4-10 binds to the membrane Hyal-2 of spleen Z cells and activates the Hyal-2/WWOX/SMAD4 signaling for cytotoxic Z cell activation to kill cancer cells. Stimulation of membrane WWOX in the signaling complex by a WWOX epitope peptide, WWOX7-21, is likely to activate the signaling. Here, mice receiving Zfra4-10 or WWOX7-21 peptide alone exhibited an increased binding of endogenous tumor suppressor WWOX with ERK, C1qBP, NF-κB, Iba1, p21, CD133, JNK1, COX2, Oct4, and GFAP in the spleen, brain, and/or lung which led to cancer suppression. However, when in combination, Zfra4-10 and WWOX7-21 reduced the binding of WWOX with target proteins and allowed tumor growth in vivo. In addition to Zfra4-10 </pubmed_abstract><journal>Cancers</journal><pubmed_title>Therapeutic Zfra4-10 or WWOX7-21 Peptide Induces Complex Formation of WWOX with Selective Protein Targets in Organs that Leads to Cancer Suppression and Spleen Cytotoxic Memory Z Cell Activation In Vivo.</pubmed_title><pmcid>PMC7464583</pmcid><funding_grant_id>106-2320-B-006-061</funding_grant_id><funding_grant_id>105–2320-B-006-046</funding_grant_id><funding_grant_id>105-2320-B-006-036</funding_grant_id><funding_grant_id>105-2320-B-006-046</funding_grant_id><funding_grant_id>107-2320-B-006-058-MY3</funding_grant_id><funding_grant_id>106–2320-B-006-061</funding_grant_id><funding_grant_id>107-2320-B-006-005</funding_grant_id><funding_grant_id>106-2320-B-006-017</funding_grant_id><funding_grant_id>106–2320-B-006-017</funding_grant_id><funding_grant_id>105–2320-B-006-036</funding_grant_id><funding_grant_id>NHRI-EX107-10734NI</funding_grant_id><pubmed_authors>Chang JY</pubmed_authors><pubmed_authors>Liu TY</pubmed_authors><pubmed_authors>Kuo HL</pubmed_authors><pubmed_authors>Chen YA</pubmed_authors><pubmed_authors>Lee MH</pubmed_authors><pubmed_authors>Huang SS</pubmed_authors><pubmed_authors>Lin SR</pubmed_authors><pubmed_authors>Ho PC</pubmed_authors><pubmed_authors>Subhan D</pubmed_authors><pubmed_authors>Wu CY</pubmed_authors><pubmed_authors>Lu CY</pubmed_authors><pubmed_authors>Chang NS</pubmed_authors><pubmed_authors>Sze CI</pubmed_authors><pubmed_authors>Su WP</pubmed_authors><pubmed_authors>Wang WJ</pubmed_authors><pubmed_authors>Chiang MF</pubmed_authors><pubmed_authors>Chen YJ</pubmed_authors><pubmed_authors>Wen KY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Therapeutic Zfra4-10 or WWOX7-21 Peptide Induces Complex Formation of WWOX with Selective Protein Targets in Organs that Leads to Cancer Suppression and Spleen Cytotoxic Memory Z Cell Activation In Vivo.</name><description>Synthetic Zfra4-10 and WWOX7-21 peptides strongly suppress cancer growth in vivo. Hypothetically, Zfra4-10 binds to the membrane Hyal-2 of spleen Z cells and activates the Hyal-2/WWOX/SMAD4 signaling for cytotoxic Z cell activation to kill cancer cells. Stimulation of membrane WWOX in the signaling complex by a WWOX epitope peptide, WWOX7-21, is likely to activate the signaling. Here, mice receiving Zfra4-10 or WWOX7-21 peptide alone exhibited an increased binding of endogenous tumor suppressor WWOX with ERK, C1qBP, NF-κB, Iba1, p21, CD133, JNK1, COX2, Oct4, and GFAP in the spleen, brain, and/or lung which led to cancer suppression. However, when in combination, Zfra4-10 and WWOX7-21 reduced the binding of WWOX with target proteins and allowed tumor growth in vivo. In addition to Zfra4-10 </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Aug</publication><modification>2026-04-07T21:58:39.552Z</modification><creation>2020-09-09T07:09:01Z</creation></dates><accession>S-EPMC7464583</accession><cross_references><pubmed>32764489</pubmed><doi>10.3390/cancers12082189</doi></cross_references></HashMap>