Considered as the second deadliest disease globally, cancer has captured the attention of researchers who have been trying with perseverance to decode its hidden aspects, to find new prognosis methods, and to develop better and more effective treatments. Plants have continuously offered an excess of unique secondary metabolites with remarkable biological applications. Alkaloids, one of the most abundant metabolites, constitute a large conglomerate of basic heterocyclic nitrogen-containing natural compounds which are normally produced by plants as toxic substances. Out of the 27,000 different alkaloids, more than 17,000 have displayed diversified pharmacological properties including anticancer activities. These metabolites have been classified either according to their chemical structures or their taxonomic origin. None of the researched alkaloids have been classified according to their molecular mechanism of action against cancer. In fact, only a fraction of the tremendous number of anticancer alkaloids has been copiously mentioned in journals. Here, we aim to provide a summary of the literature on some of the promising anticancer alkaloids that have not been well discussed previously and to classify them according to their molecular mechanisms of action. This review will provide a better understanding of the anticancer mechanisms of these promising natural products that are a rich reservoir for drug discovery.

https://www.mdpi.com/1420-3049/22/2/250/pdf

Emerging Cytotoxic Alkaloids in the Battle against Cancer: Overview of Molecular Mechanisms.

Oxymatrine (OMT) is a major alkaloid found in radix Sophorae flavescentis extract and has been reported to exhibit various pharmacological activities. We elucidated the detailed molecular mechanism(s) underlying the therapeutic actions of OMT in non-small cell lung cancer (NSCLC) cells and a xenograft mouse model. Because the STAT5 signaling cascade has a significant role in regulating cell proliferation and survival in tumor cells, we hypothesized that OMT may disrupt this signaling cascade to exert its anticancer effects. We found that OMT can inhibit the constitutive activation of STAT5 by suppressing the activation of JAK1/2 and c-Src, nuclear localization, as well as STAT5 binding to DNA in A549 cells and abrogated IL-6-induced STAT5 phosphorylation in H1299 cells. We also report that a sub-optimal concentration of OMT when used in combination with a low dose of paclitaxel produced significant anti-cancer effects by inhibiting cell proliferation and causing substantial apoptosis. In a preclinical lung cancer mouse model, OMT when used in combination with paclitaxel produced a significant reduction in tumor volume. These results suggest that OMT in combination with paclitaxel can cause an attenuation of lung cancer growth both in vitro and in vivo.

https://www.mdpi.com/2072-6694/11/1/49/pdf

Oxymatrine Attenuates Tumor Growth and Deactivates STAT5 Signaling in a Lung Cancer Xenograft Model

Sophora alopecuroides L.: An ethnopharmacological, phytochemical, and pharmacological review

Quinolizidine alkaloids derivatives from Sophora alopecuroides Linn: Bioactivities, structure-activity relationships and preliminary molecular mechanisms.

Background In spite of major technological advances in conventional therapies, cancer continues to remain the leading cause of mortality worldwide. Phytochemicals are gradually emerging as a rich source of effective but safer agents against many life-threatening diseases. Methods Various phytochemicals with reported anticancer activity have been simply categorized into major phytoconstituents- alkaloids, polyphenols, saponins, tannins and terpenoids. Results The adverse effects associated with currently available anticancer medications may be overcome by using plant-derived compounds either alone or in combination. Exploration of plant kingdom may provide new leads for the accelerated development of new anticancer agents. Conclusion Although numerous potent synthetic drugs have been introduced for cancer chemotherapy, yet their serious toxicity concerns to normal cells apart from drug resistance have emerged as the major obstacles for their clinical utility over a prolonged duration of time. Current status and potential of phytochemicals and their derivatives in cancer therapy have been briefly reviewed in the present manuscript.

Phytochemicals in Anticancer Drug Development

UNLABELLED The aim of this study was to explore the effects of oxymatrine in treating breast cancer patients using biomolecular methodology. Human breast cancer MCF-7 cells were treated with oxymatrine at concentrations of 0 (control), 25, 50 and 100 µg/mL. Apoptosis assay by Annexin/PI staining was performed to examine the effects of oxymatrine on apoptotic rates of MCF-7 cells at time points of 24 h, 48 h, and 72 h after treatment. Real-time PCR was performed for the mRNA abundance of Bax and Bcl-2 after the cells were treated with oxymatrine at concentration of 0, 25, 50, and 100 µg/mL at the time points of 24, 48, and 72 h. Western blotting was performed when the cells were treated with oxymatrine at various concentrations for 72h. High concentration of oxymatrine at 100 µg/mL enhanced apoptosis by 6.4-fold at 72 h compared with control (33.16% vs. 4.47%; t= 9.82, p< 0.001). Oxymatrine at 100 µg/mL up regulated Bax mRNA abundance by 169 % at 72 h (t = 18.32, p = 0.001), and reduced Bcl-2 mRNA abundance by 24 % at 72 h (t = 6.30, p = 0.001) compared with control. Oxymatrine enhanced the expression of Bax protein while reduced the expression of Bcl-2 protein. Oxymatrine treatment showed pro-apoptotic effects in breast cancer MCF-7 cells, and these effects correlated with the up regulation of Bax transcription and protein expression and the down regulation of Bcl-2 transcription and protein expression in a time- and dose-dependent manner. CONCLUSION Oxymatrine had effects in promoting apoptosis in human breast cancer MCF-7 cells by mediating the mRNA and protein expression levels of Bax and Bcl-2.

Oxymatrine mediates Bax and Bcl-2 expression in human breast cancer MCF-7 cells.

We investigated the role of the transcriptional mediator subunit 23 (MED23) in everolimus drug resistance, invasion and metastasis during breast cancer treatment and its molecular mechanism. We also evaluated the endocrinotherapy and prevention method for breast cancer. Breast cancer cell strains were established that can continuously express MED23, as well as inducible MED23-shRNA expression plasmids. The inductive agent, doxycycline (Dox), was added to the water for long-term silencing of MED23 in intratumoral cells. We conducted experiments on the role of MED23 in the regulation of invasion and metastasis of breast cancer using cell culture, western blotting, MTT proliferation experiment, fluorescent quantitative PCR and chromatin immunoprecipitation (ChIP). The silencing of MED23 significantly inhibited cellular growth and proliferation as well as soft agar cloning. Silencing of MED23 strengthened the sensitivity of the everolimus-resistant breast cancer cell strains BT474 and MCF-7/ADM cells to everolimus medication. The silencing of MED23, in combination with everolimus, inhibits the cell cycle progress of breast cancer cells. ChIP indicated that the mutual regulation of HER2 and MED23 also participates in the formation of the everolimus drug resistance mechanism. Therefore, MED23 plays an important role in everolimus drug resistance, invasion, and metastasis of breast cancer. As a potential molecular therapeutic target of breast cancer, MED23 overcomes drug resistance in clinical endocrinotherapy and controls the distal relapse and metastasis in breast cancer by the targeted silencing of MED23.

/pdf/med23-in-endocrinotherapy-for-breast-cancer-53gk2gy9a7.pdf

MED23 in endocrinotherapy for breast cancer

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Dinuo Li

Author Tools

Chat about Author

Papers

Oxymatrine mediates Bax and Bcl-2 expression in human breast cancer MCF-7 cells.

MED23 in endocrinotherapy for breast cancer