{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:44:15Z","timestamp":1786977855067,"version":"build-2736575974"},"reference-count":43,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2018,12,18]],"date-time":"2018-12-18T00:00:00Z","timestamp":1545091200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Carl and Leonora Fingerhut Fund Foundation of the Sackler Faculty of Medicine, Tel Aviv University, Israel"},{"name":"Djerassi-Elias Institute of Oncology Tel Aviv University, Israel."}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:p>The extracellular matrix (ECM) affects cancer cell characteristics. Inability of normal epithelial cells to attach to the ECM induces apoptosis (anoikis). Cancer cells are often anoikis resistant, a prerequisite for their metastatic spread. Previously we demonstrated that the placenta manipulates its surrounding ECM in a way that prevents breast cancer cells (BCCL) attachment and induces their motility and aggregation. This fits with the fact that although breast cancer during pregnancy is often advanced, metastasis to the placenta is rarely observed. Placental intervillous space provides suitable conditions for cancer cell arrival. Yet, the outcome of the short communication between the placental ECM to the BCCL and its effect on BCCL malignant potential are unknown, and are the focus of our study. In the current study we analyzed the effect of placental ECM on BCCL survival pathways and drug resistance. Microarray analysis suggested activation of the NF\u2010\u03baB and stress response pathways. Indeed, the placenta\u2010conditioned ECM induced autophagy in ER\u03b1 + BCCL, inactivated the NF\u2010\u03baB inhibitor (I\u03baB) and increased integrin \u03b15 in the BCCL. The autophagy mediated MCF\u20107 and T47D migration and the placental ECM\u2010BCCL interactions reduced the BCCL sensitivity to Taxol. We also demonstrated by using siRNA that integrin \u03b15 was responsible for the MCF\u20107 autophagy and suggest this molecule as a suitable target for therapy.<\/jats:p>","DOI":"10.1002\/ijc.31861","type":"journal-article","created":{"date-parts":[[2018,9,8]],"date-time":"2018-09-08T11:48:25Z","timestamp":1536407305000},"page":"1633-1644","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Placenta\u2010conditioned extracellular matrix (ECM) activates breast cancer cell survival mechanisms: A key for future distant metastases"],"prefix":"10.1002","volume":"144","author":[{"given":"Oded","family":"Komemi","sequence":"first","affiliation":[{"name":"Oncogenetic Laboratory Meir Medical Center  Kfar Saba Israel"},{"name":"Sackler Faculty of Medicine Tel Aviv University  Tel Aviv Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gali 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