184 Neurotensin-polyplex as a Potential Tool in Gene Therapy for Human Breast Cancer

Castillo-Rodríguez, Rosa Angélica; Arango-Rodríguez, Martha L.; Escobedo, Luis G.; Rubio-Zapata, Héctor; Tellez-Lopez, Víctor M.; Mejía-Castillo, Teresa; Dupouy, Sandra; Forgez, Patricia; Martínez‐Fong, Daniel

doi:10.1016/s0959-8049(12)70252-6

Cited by 2 publications

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“…In the study of Heakal et al, nanoliposomal short-chain ceramide, a chemical that can inhibit agonist-dependent translocation of NTSR1, was found to significantly inhibit NTSR1-mediated MDA-MB-231 breast cancer progression (mitogenesis, migration, and matrix metalloproteinase activity) [8]. Castillo-Rodriguez et al recently developed a neurotensinpolyplex that transfects therapeutic genes into NTSR1expressing breast cancer cells (MDA-MB-231 cells) and kills tumor cells in both in vitro and in vivo models [20]. Unfortunately, to the best knowledge of the authors, a clinically usable NTSR1 antagonist is still not available.…”

Section: Discussionmentioning

confidence: 99%

Neurotensin Receptor 1 (NTSR1) Overexpression in Breast Carcinomas Is Common and Independent of ER/PR/Her2 Expression

Gui¹,

Liu²,

Meng³

et al. 2013

JCT

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Neurotensin (NT) is a 13-amino acid peptide with trophic effects on some neoplasms. Its bioactivities are mainly mediated by neurotensin receptor 1 (NTSR1). Both NT and NTSR1 were found to be upregulated in breast cancer. NT/NTSR1 thus becomes a potential therapeutic target. We studied whether any correlation exists between the expression of NTSR1 in breast carcinomas and the expression of ER, PR, and Her2. A total 85 cases of invasive ductal (62) and lobular (23) breast carcinomas were studied. Based on their ER/PR profiles, the ductal carcinomas (DCs) were subcategorized into ER+/PR+ (21), ER+/PR﹣ (20), and ER﹣/PR﹣ (21). All of the lobular carcinomas (LCs) were ER+/PR+. 21.57% of all DCs and 5.56% of LCs were Her2 positive. 77.78% of ER﹣/PR﹣ DCs were also Her2 negative (triple negative). The expression of NTSR1 was detected by immunohistochemistry and was semiquantitated (as negative, 1+, 2+, 3+). Both 2+ and 3+ were collectively defined as overexpression. The expression of NTSR1 was weak and focal in non-neoplastic mammary epithelial cells. It is increased in 74.19% of DCs (80.95% in ER+/PR+, 75% in ER+/PR﹣, and 66.67% in ER﹣/PR﹣ group), and in 95.65% of LCs. The overexpression of NTSR1 is similar between ER+ DCs and ER﹣ DCs (75% vs 66.67%, p > 0.05) as well as between PR+ DCs and PR﹣ DCs (80.95% in ER+/PR+ DCs vs 75% in ER+/PR﹣ DCs, p > 0.05). And it was seen in 77.78% of Her2+ DCs, 78.38% of Her2﹣ DCs, 94.12% of Her2﹣ LCs, and 78.57% of triple negative DCs. Overall, NTSR1 is commonly overexpressed in both ductal and lobular breast carcinomas and is independent of the ER/PR/Her2 profiles of the tumors. The present data supports the potential benefit of developing NTSR1 blockers in the adjuvant therapy of breast carcinomas, particularly for those “triple negative” tumors.