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Synthesis of potent MDA-MB 231 breast cancer drug molecules from single step.

ABSTRACT: We have prepared novel potent breast cancer drug molecules from non-toxic and inexpensive method. Column chromatography is not necessary for purification of target molecules. The value of overall atom economy, environmental factor, environmental catalyst and product mass intensity gives additional merits for this synthetic method. Synthesized flexible dimeric imidazolium bromides showed less toxicity and gives excellent anticancer response against normal mammary epithelial cells. Novel dimeric pyridinium bromides showed excellent anticancer response against tested cancer cell lines. In cell cycle, novel flexible dimeric pyridinium bromides showed significant arrest in the G2/M phase by nearly three folds, when compared with control drug. We have studied the targeting epidermal growth factor receptor for all the synthesized flexible amino substituted and methyl substituted dimeric pyridinium bromides.

SUBMITTER: Govindaraj S

PROVIDER: S-EPMC10600176 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature

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Synthesis of potent MDA-MB 231 breast cancer drug molecules from single step.

Govindaraj Senthilnathan S Ganesan Kilivelu K Dharmasivam Mahendiran M Raman Lakshmisundaram L Alam Mohammed Mujahid MM Amanullah Mohammed M

Scientific reports 20231025 1

We have prepared novel potent breast cancer drug molecules from non-toxic and inexpensive method. Column chromatography is not necessary for purification of target molecules. The value of overall atom economy, environmental factor, environmental catalyst and product mass intensity gives additional merits for this synthetic method. Synthesized flexible dimeric imidazolium bromides showed less toxicity and gives excellent anticancer response against normal mammary epithelial cells. Novel dimeric p ...[more]

PMID: 37880270

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MDA-MB-231 breast cancer cells overexpressing single VEGF isoforms display distinct colonisation characteristics.

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| S-EPMC4559830 | biostudies-literature

Effects of FSTL1 on cell proliferation in breast cancer cell line MDA‑MB‑231 and its brain metastatic variant MDA‑MB‑231‑BR.

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| S-EPMC11013444 | biostudies-literature

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| S-EPMC5369870 | biostudies-literature

Allyl Isothiocyanate Exhibits No Anticancer Activity in MDA-MB-231 Breast Cancer Cells.

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| S-EPMC5796094 | biostudies-literature

Effects of osteopontin inhibition on radiosensitivity of MDA-MB-231 breast cancer cells.

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| S-EPMC2949679 | biostudies-literature

Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

Project description:Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abolishment of apoptosis and cytotoxicity in pre-treated MDA-MB-231 cells. In contrast, artesunate was more cytotoxic towards the less tumorigenic MDA-MB-468 cells without showing resistance. Unraveling the underlying molecular mechanisms, we found that resistance was induced due to activation of the tumor progression related transcription factors NFκB and AP-1. Thereby transcription, expression and activity of the matrix-degrading enzyme MMP-1, whose function is correlated with increased invasion and metastasis, was up-regulated upon acquisition of resistance. Additionally, activation of the apoptosis-related factor NFκB lead to increased expression of ant-apoptotic bcl2 and reduced expression of pro-apoptotic bax. Application of artesunate in vivo in a model of xenografted breast cancer showed, that tumors growth was not efficiently abolished as compared to the control drug doxorubicin. Taken together our in vitro and in vivo results correlate well showing for the first time that artesunate induces resistance in highly metastatic breast tumors.

| S-EPMC3102747 | biostudies-literature

MEKK2 regulates paxillin ubiquitylation and localization in MDA-MB 231 breast cancer cells.

Project description:The intracellular kinase MEKK2 (mitogen-activated protein kinase/extracellular-signal-regulated kinase kinase kinase 2) is an upstream regulator of JNK (c-Jun N-terminal kinase), but additional functions for MEKK2 have not been well defined. Silencing MEKK2 expression in invasive breast tumour cells markedly inhibits xenograft metastasis, indicating that MEKK2 controls tumour cell function required for tumour progression. In our previous investigation of MEKK2 function, we discovered that tumour cell attachment to fibronectin recruits MEKK2 to focal adhesion complexes, and that MEKK2 knockdown is associated with stabilized focal adhesions and significant inhibition of tumour cell migration. In the present study we investigate MEKK2 function in focal adhesions and we report that MEKK2 physically associates with the LD1 motif of the focal adhesion protein paxillin. We reveal that MEKK2 induces paxillin ubiquitylation, and that this function requires both the paxillin LD1 motif and MEKK2 kinase activity. Finally, we demonstrate that MEKK2 promotes paxillin redistribution from focal adhesions into the cytoplasm, but does not promote paxillin degradation. Taken together, our results reveal a novel function for MEKK2 as a regulator of ubiquitylation-dependent paxillin redistribution in breast tumour cells.

| S-EPMC4467534 | biostudies-literature

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