scholarly journals Tumor Targeting by Conditioned Medium Derived From Human Amniotic Membrane: New Insight in Breast Cancer Therapy

2021 ◽  
Vol 20 ◽  
pp. 153303382110363
Author(s):  
Ameneh Jafari ◽  
Mostafa Rezaei-Tavirani ◽  
Hassan Niknejad ◽  
Hakimeh Zali

Objectives: Traditional breast cancer treatments have challenges including inefficiency, multidrug resistance, severe side effects, and targeting non-specifically. The development of alternative treatment strategies has attracted a great deal of interest. Using the amniotic membrane has become a promising and convenient new approach for cancer therapy. This study aimed to evaluate the anti-cancer ability of conditioned medium extracted from the human amniotic membrane (hAM-CM) on breast cancer cells. Methods: Conditioned medium was collected after 48 h incubation of hAM in epithelial up manner. MTT, cell cycle, apoptosis, colony formation, and sphere assays were used to determine the impact of hAM-CM on breast cancer cell lines. The effects of hAM-CM on the migration and invasion of breast cancer cells were determined using scratch wound healing and transwell assays, respectively. Results: Based on the results, cell viability was significantly decreased by hAM-CM in a dose-dependent manner. The hAM-CM remarkably induced apoptosis and necrosis of cancer cells. Moreover, cell migration and invasion potential of cancer cells decreased after the hAM-CM treatment. Further, both the number of colonies and their morphologies were affected by the treatment. In the treated group, a significant decrease in the number of colonies along with an obvious change in their morphologies from holoclone shape to a dominant paracolone structure was observed. Conclusion: Our results indicate that the conditioned medium derived from the human amniotic membrane able to inhibit proliferation and metastasis of tumor cells and can be considered a natural and valuable candidate for breast cancer therapy.

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 277 ◽  
Author(s):  
Xin-Ying Qu ◽  
Jin-Wei Ren ◽  
Ai-Hong Peng ◽  
Shi-Qi Lin ◽  
Dan-Dan Lu ◽  
...  

Four angucycline glycosides were previously characterized from marine-derived Streptomyces sp. OC1610.4. Further investigation of this strain cultured on different fermentation media from that used previously resulted in the isolation of two new angucycline glycosides, vineomycins E and F (1–2), and five known homologues, grincamycin L (3), vineomycinone B2 (4), fridamycin D (5), moromycin B (7), and saquayamycin B1 (8). Vineomycin F (2) contains an unusual ring-cleavage deoxy sugar. All the angucycline glycosides isolated from Streptomyces sp. OC1610.4 were evaluated for their cytotoxic activity against breast cancer cells MCF-7, MDA-MB-231, and BT-474. Moromycin B (7), saquayamycin B1 (8), and saquayamycin B (9) displayed potent anti-proliferation against the tested cell lines, with IC50 values ranging from 0.16 to 0.67 μM. Saquayamycin B (9) inhibited the migration and invasion of MDA-MB-231 cells in a dose-dependent manner, as detected by Transwell and wound-healing assays.


MedChemComm ◽  
2015 ◽  
Vol 6 (5) ◽  
pp. 778-787 ◽  
Author(s):  
Kavita Yadav ◽  
Priyanshu Bhargava ◽  
Sandhya Bansal ◽  
Manish Singh ◽  
Siddhi Gupta ◽  
...  

Anticancer drug Tamoxifen is modified to charged lithocholic acid derived amphiphile for enhanced cytotoxicity against breast cancer cells.


2021 ◽  
Vol 14 ◽  
Author(s):  
Farid Hashemi ◽  
Ali Zarrabi ◽  
Amirhossein Zabolian ◽  
Hossein Saleki ◽  
Mahdi Vasheghani Farahani ◽  
...  

Breast cancer is one of the leading causes of death worldwide. Breast cancer cells demonstrate uncontrolled proliferation, and high metastatic capacity. They can obtain resistance to chemotherapy and radiotherapy. This has resulted in troublesome problems in its treatment. Nature as a rich source of plant derived-natural products with anti-tumor activity can be of interest in breast cancer therapy. Ginsenosides are triterpenoid saponins and considered as secondary metabolites exclusively found in Panax species. From immemorial times, ginsenosides have been applied in treatment of various disorders such as diabetes, inflammatory diseases, neurological disorders, and particularly, cancer. In the present review, we highlight anti-tumor activity of ginsenosides against breast cancer cells. Ginsenosides are able to induce apoptosis and cell cycle arrest. They interfere with breast cancer metastasis via inhibiting epithelial-to-mesenchymal transition, matrix metalloproteinase proteins and angiogenesis. Ginsenosides can promote efficacy of chemotherapy via suppressing migration and proliferation. Molecular pathways such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), insulin-like growth factor-1, Wnt, microRNAs and long non-coding RNAs are affected by ginsenosides in suppressing breast cancer malignancy. Consequently, ginsenosides are versatile compounds in breast cancer therapy by suppressing growth, and invasion, as well as promoting their sensitivity to chemotherapy.


2019 ◽  
Vol 8 (11) ◽  
pp. 1539-1552 ◽  
Author(s):  
Juan Carlos Juárez-Cruz ◽  
Miriam Daniela Zuñiga-Eulogio ◽  
Monserrat Olea-Flores ◽  
Eduardo Castañeda-Saucedo ◽  
Miguel Ángel Mendoza-Catalán ◽  
...  

Breast cancer is the most common invasive neoplasia, and the second leading cause of the cancer deaths in women worldwide. Mammary tumorigenesis is severely linked to obesity, one potential connection is leptin. Leptin is a hormone secreted by adipocytes, which contributes to the progression of breast cancer. Cell migration, metalloproteases secretion, and invasion are cellular processes associated with various stages of metastasis. These processes are regulated by the kinases FAK and Src. In this study, we utilized the breast cancer cell lines MCF7 and MDA-MB-231 to determine the effect of leptin on FAK and Src kinases activation, cell migration, metalloprotease secretion, and invasion. We found that leptin activates FAK and Src and induces the localization of FAK to the focal adhesions. Interestingly, leptin promotes the activation of FAK through a Src- and STAT3-dependent canonical pathway. Specific inhibitors of FAK, Src and STAT3 showed that the effect exerted by leptin in cell migration in breast cancer cells is dependent on these proteins. Moreover, we established that leptin promotes the secretion of the extracellular matrix remodelers, MMP-2 and MMP-9 and invasion in a FAK and Src-dependent manner. Our findings strongly suggest that leptin promotes the development of a more aggressive invasive phenotype in mammary cancer cells.


2021 ◽  
Vol 45 (8) ◽  
pp. 4032-4045
Author(s):  
Diego Cadena Castro ◽  
Gerardo Gatti ◽  
Sandra E. Martín ◽  
Paula M. Uberman ◽  
Mónica C. García

Improved efficacy and safety of tamoxifen-loaded hybrid nanocarriers based on Fe3O4 nanoparticles, l-cysteine and hyaluronic acid for breast cancer therapy.


Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 546
Author(s):  
Rémi Cousin ◽  
Hugo Groult ◽  
Chanez Manseur ◽  
Romain Ferru-Clément ◽  
Mario Gani ◽  
...  

Sugar-based molecules such as heparins or natural heparan sulfate polysaccharides have been developed and widely studied for controlling heparanase (HPSE) enzymatic activity, a key player in extracellular matrix remodelling during cancer pathogenesis. However, non-enzymatic functions of HPSE have also been described in tumour mechanisms. Given their versatile properties, we hypothesized that sugar-based inhibitors may interfere with enzymatic but also non-enzymatic HPSE activities. In this work, we assessed the effects of an original marine λ-carrageenan derived oligosaccharide (λ-CO) we previously described, along with those of its native counterpart and heparins, on cell viability, proliferation, migration, and invasion of MDA-MB-231 breast cancer cells but also of sh-MDA-MB-231 cells, in which the expression of HPSE was selectively downregulated. We observed no cytotoxic and no anti-proliferative effects of our compounds but surprisingly λ-CO was the most efficient to reduce cell migration and invasion compared with heparins, and in a HPSE-dependent manner. We provided evidence that λ-CO tightly controlled a HPSE/MMP-14/MMP-2 axis, leading to reduced MMP-2 activity. Altogether, this study highlights λ-CO as a potent HPSE “modulator” capable of reducing not only the enzymatic activity of HPSE but also the functions controlled by the HPSE levels.


2013 ◽  
Vol 41 (01) ◽  
pp. 177-196 ◽  
Author(s):  
Shengpeng Wang ◽  
Zhangfeng Zhong ◽  
Jianbo Wan ◽  
Wen Tan ◽  
Guosheng Wu ◽  
...  

Oridonin, a natural tetracycline diterpenoid isolated from Chinese herb Rabdosia rubescens, has been reported to be a potent cytotoxic agent against a wide variety of tumors. However, its effect on highly metastatic breast cancer cells has not been addressed. In this study, we investigated the effects of oridonin on growth, migration and invasion of highly-metastatic human breast cancer cells. Our results showed that oridonin induced potent growth inhibition on human breast cancer cells MCF-7 and MDA-MB-231 in a time- and dose-dependent manner. According to the flow cytometric analysis, oridonin suppressed MCF-7 cell growth by cell cycle arrest at the G2/M phase and caused accumulation of MDA-MB-231 cells in the Sub-G1 phase. The induced apoptotic effect of oridonin was further confirmed by a morphologic characteristics assay and TUNEL assay. Oridonin triggered the reduction of Bcl-2/Bax ratio, caspase-8, NF-κB (p65), IKKα, IKKβ, phospho-mTOR, and increased expression level of cleaved PARP, Fas and PPARγ in a time-dependent manner. Immunofluorescent analysis showed that γH2AX-containing nuclear foci were significant in oridonin-treated MDA-MB-231 cells. Meanwhile, oridonin significantly suppressed MDA-MB-231 cell migration and invasion, decreased MMP-2/MMP-9 activation and inhibited the expression of Integrin β1 and FAK. In conclusion, oridonin inhibited the growth and induced apoptosis in breast cancer cells, which might be related to DNA damage and activation of intrinsic or extrinsic apoptotic pathways. Moreover, oridonin also inhibited tumor invasion and metastasis in vitro possibly via decreasing the expression of MMPs and regulating the Integrin β1/FAK pathway in MDA-MB-231 cells.


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