THE ANTICANCER ACTIVITY OF BIOACTIVE COMPOUNDS FROM MEDICINAL PLANTS: AN REVIEWHTML Full Text
THE ANTICANCER ACTIVITY OF BIOACTIVE COMPOUNDS FROM MEDICINAL PLANTS: AN REVIEW
University Institute of Biotechnology, Chandigarh University, Gharuan, Mohali - 140413, Punjab, India.
ABSTRACT: Cancer is a serious health concern in both developed and developing nations. Cancer causes due to unwanted growth of cells and irregular cell division. Medicinal plants have been used by village folk from ancient times. The plants contain various bioactive compounds that can be used for treating cancer. Some of the phyto compounds isolated from plants have shown promising results; these include curcumin, vinblastine, vincristine, camptothecin. The various phytochemicals like terpenoid, flavonoids, and coumarins were also found promising in treating cancer. A lot of plants based compounds are under trial resulted in good responses. Around 17 different plant families, members with their active constituents reported for targeting cancer pathways were summarized. In this review, various medicinal plants which are reported for anticancer drug discovery were listed and mentioned for their mechanisms of action, such as CDK inhibitor, roles of apoptosis, and angiogenesis in cancer pathways. These plants are very useful in various research studies or for research purposes; these plants seek considerable attention.
Anticancer, Medicinal plant, Bioactive compound, Phytochemical
INTRODUCTION: Cancer cells are the cells that do not follow normal signals that ensure correct cellular growth and death. When normal cells acquire unlimited replication potential and proliferation. Cancer cells originate within normal cells as irregular masses and then convert these cells into malignant cells. Cancer is the disease of the cell cycle; irregularity in cell cycle machinery are major causes of cancerous growth. ICMR registry data, the new cancer cases in India is estimated to rise to 1·45 million each year 1. Cases will rise to nearly 1.80 million by 2025 2. The first documented record on medicinal plants dates back to 2600 B.C. in Mesopotamia, consisting of around 1000 drugs of plant origin 3.
According to National Cancer Institute (NCI) screening results, about 3,000 plant species were showing anticancer activity 4. Around 25000 plants were screened by pharmaceutical companies, and most of the drugs that are available in the market are plant-derived natural products 5. WHO reports indicate that more than 80% of the world’s population is dependent on traditional drugs, made up of natural compounds 6.
Different types of anticancer drugs which are available in the market for treating cancer are beyond the reach of common people 7. These bioactive compounds from plants protect the patients by triggering various biological responses. Some of the responses modulate the activity of the enzyme and proteins having a specific role in cancer biology 8. The plant-derived bioactive compounds have been reported to target the different pathways that lead to cancer; their target includes CDK inhibitors, apoptosis, and NF-κB pathways 9. How various genes and protein leads to the normal functioning of the cell are described below.
CDK Inhibitor: The process of replication and dividing of the cell is regulated by different protein complexes. Among such complexes, Cyclin-dependent kinases (CDK) and cyclin play a major role in the transition from one phase to the other phase of cell cycle 10. The cell cycle checkpoint ensures proper DNA replication and chromosome segregation. If some part of DNA is damaged or mutated, signals are relayed to checkpoints machinery to stop the process of replication until it is repaired 11. The relation between cell cycle machinery and checkpoints is clear, as it leads to unlimited cell proliferation leading to cancer 12. The cell cycle is a tightly regulated process, CDK combines with cyclin to form a complex. Each cyclin is phosphorylated by activated by the kinase activity of CDK 13. Then CDK cyclin complexes phosphorylate specific substrates to activate DNA synthesis (G1/S phase) and the structural components that help in mitosis (G2/M phase) 14.
Apoptosis: Cancer cells inhibit apoptosis by various genetic changes in the humans body. Thus plant-based compounds that can trigger apoptosis in cancerous cells can be considered a potential candidate for the development of drugs 15. P53 is a tumor suppressor gene that maintains the integrity of the cell genome. If cells sense a DNA damage signal, P53 directs the cell for repair pathways 16. MDM2 (Murine double minute 2) acts as a negative regulator of p53; both proteins are present in the complex form normally. The appearance of DNA damage induces the phosphorylation of p53, thus breaking the binding of p53-MDM2 complex 17. P53 operates by regulation of CDK inhibitor (p21), which inhibits the activity of cyclin and arresting the cell cycle 18. In cancerous cells, apoptosis is inhibited by the anti-apoptotic protein Bcl-2, which helps in the regulation of caspases that activate apoptosis. Bax protein inhibits Bcl-2 function and acts as a pro-apoptotic protein that activates caspases and cell death 19.
Angiogenesis Inhibitors: Angiogenesis is the physiological process through which new blood vessels are originated, it is enhanced in most cancer cells. Hence plant-based compounds that inhibit angiogenesis can be used for treating cancer 20.
Signaling Pathways Related to Cancer: NF-κB represents the transcriptional factors that are associated with the expression of various genes responsible for angiogenesis, proliferation, apoptosis, and metastasis 21. The natural compounds that can target NF-κB and its regulated gene expressions might prove useful for cancer therapy 22.NF-κBshows its effect by inhibiting p-IκB-α, which causes induction of NF-κB associated gene expressions such as Bcl-xl and Bcl-2 23. These proteins are having a role in apoptosis pathways.
Current Anti-cancer Drugs are Associated with Side Effects: Chemotherapy drugs act on fast-growing cells, that can’t differentiate between cancer and normal cells. Current drugs used in chemotherapy have shown adverse effects on normal cells of patients. So there is an increased need for active constituents with lesser side effects 24.
Natural Medicine for Cancer Therapy: In the last few decades, medicinal plants have been proved a great source for pharmaceutically active compounds 25. The anti-cancer phytochemicals and structural derivatives residing in plants are promising resources for improved and less toxic cancer therapy 26.
The names of the plants having anti-cancer properties were identified from the book “Medicinal and Aromatic Plants of Himachal Pradesh” by Narain Singh Chauhan. Then the plants were searched by entering the name of the plant along with the word anticancer. Pubmed, Google, and Science Direct were searched for the research articles to list the names of active components which have anticancer potential. The information accumulated on the active compounds and their mechanisms of action were listed in a table format.
The plants showing anti-cancer properties are listed in Table 1. along with their mechanism of action. The phenolic compounds obtained from plant extract induce apoptosis and act as anticancer agents 27. Curcumin, thymol, rosmarinic acid, β-carotene, quercetin, rutin, allicin, gingerol, epigallocatechin gallate, and coumarin exhibit anticancer potential 28. Different alkaloids were isolated from the plants include taxol and camptothecins that are used in anticancer drugs 29. A new benzylisoquinoline alkaloid was isolated from plant Annona squamosa has anticancer potential 30. Secondary metabolites like terpenoids and flavonoids showed potent anticancer effects 31. Several molecules showed an inhibitory effect on cyclins and cyclin-dependent kinases, leading to controlled cell proliferation 32. These plant-derived biomolecules arrest the cell cycle at Go/G1 phase 33, S phase 34. Withaferin A, a constituent of Withania somnifera, arrested the cells at G2 phase 35 and G2/M phase inhibition 36. Curcumol proved to be an inducer of apoptosis in cancer cell lines via targeting major signaling pathways, including MAPK/ERK, PI3K/Akt, and NF-Κb. Table 1.
Cancer Cell Lines Used: Allicin inhibited the proliferation and induces glioma cell by affecting Bcl‑2‑associated, protein expression thus acted like an apoptosis inhibitor. Vinblastine was found to induce DNA-binding activities of the transcription factor NF-κB. α -thujone, 1,8-cineole, and camphor increased the ratio of Bax/Bcl2 as an apoptotic index leading to apoptosis in MCF7 cells (breast carcinoma) and HeLa cells (cervical carcinoma). The various bioactive compounds of plant origin and their targets were summarized in Table 1.
TABLE 1: PLANTS HAVING ANTI-CANCER PROPERTIES AND THEIR MECHANISM OF ACTION
|S. no.||Botanical Name/ Family||Plant bioactive compound||Plant
|Test cell lines used||Conc.||Molecular mechanism of action|
(hepatic stellate cells)
|30 μM||Apoptosis and effect on signaling pathways, MAPK/ERK, PI3K/Akt and NF-κB 37|
|Alliin||Bulb||Multiple myeloma cell lines, RPMI-8226 and JJN3||------||MAPK and PI3K inhibitors, apoptosis 38,39|
|Vinblastine||Leaves||Jurkat Leukaemic T-cells||10, 500 and 1000 μg/ml||Apoptosis,( induces the DNA-binding activities of the transcription factor NF-κB40, 41|
|Sideroxylonal B and macrocarpal A||Leaves||MCF7 (breast carcinoma cell line), HEP2 (laryngeal carcinoma), CaCo(colonic adenocarcinoma)||MCF7 (IC50 = 4.4 ± 0.25 μg mL−1) and CaCo cell line (IC50 = 4 ± 0.36 μg mL−1)||S-phase specific effects.
|Colchicine||Seeds||A549 and MDA-MB231 cell lines||60 nM||microtubule destabilization, G2/M phase, and triggering apoptosis 44, 45|
|Phenolics/flavanoids||Leaves||MCF-7 (Human mammary gland adenocarcinoma) and A-549 (Human lung cancer cell line)||643.13 ± 4.2 μg/ml||Cytotoxic effect, regulating the Bcl-2 family protein expression, leading to apoptosis 46, 47|
|Hyperforin||Flower||MT-450 mammary carcinoma cells, AMP-activated protein kinase (AMPK) and decreased the expression of mammalian target of rapamycin (p-mTOR)||3–15 μM||increased the activity of caspase-9 and caspase-3 Apoptosis, colorectal cancer Inhibiting AMPK/mTOR pathway 48, 49, 50|
|Roscovitine||Rhizome||Breast cancer cells MDA-MB231||10 μg/mL||Inhibitory effect on cyclin-dependent kinase (CDK) activity, caused cell-cycle inhibition in the G1 and G2 phasesapoptosis51, 52|
|Cannabidiol||Leaves||Human gastric cancer SGC-7901 cells||23.4 μg/mL||cell cycle arrest at the G0–G1 phase, decreased Bcl-2 expression levels, apoptosis 53, 54|
|Catechins||Leaves||Caco-2 cancer cell line||800 μg/ml||Levels of aquaporin 5 protein decreased, apoptosis 55, 56|
|Terpinene-4-ol, α-terpineol, and safrole camphor||Leaves||Human A549, lung cancer, and MCF-7,
Breast cancer cells.
|50 µg/ml||induced up-regulation of cell-cycle related proteins P53 and P21.57, 58|
|Zingerone||Rhizome||BALB/c mouse-tumor model||2 mM||decreased cyclinD1 expression, mitotic arrest, Suppresses angiogenesis 59, 60|
|α -thujone, 1,8-cineole, and camphor||Essential oil||LNCaP cells (prostate carcinoma),
MCF7 cells (breast carcinoma) and HeLacells (cervical carcinoma)
|100 μg/mL and 200 μg/mL||Anticancer, increased the ratio of Bax/Bcl2 as an apoptotic index.61, 62|
|Coumaroyl alphitolic||Fruit||cervical OV2008 and breast MCF-7 cancer cells||0-3 mg/ml)||Enhanced expression of Bax and decreased Bcl2 63, 64
|Withanolides||Leaves||Neuroblastoma (NB cells)||2 μM||Suppression of Akt, mTOR, and NF-κB pathways 65, 66|
|Extracts||Leaves||HeLa, MCF-7||1-100 µg/µL||Upregulation of Bax gene, elevated expression of p53, apoptosis, 67,68|
|Extracts||Leaves||A549 cell line.||40.0 µg/ml)||cytotoxic effects 69, 70|
|Linalool, and linalyl acetate||Essential oil||Human prostate cancer PC-3||2.5 µM||arrested in the G2/M phase, 71, 72|
|Girinimbine||Leaves||A549 lung cancer cells||19.01
|upregulation of p53 73, 74|
|Limonoids||Seed||HL60 leukemia cells||2.7−3.1 μM||activated caspases-3, -8, and -9 apoptosis 75, 76|
|α-santalol||Essential oil||Human melanoma UACC-62||50 μM-100 μM||G2/M phase arrest and apoptosis 77, 78|
|Leaves||Human cancer cell lines (JFCR-39)||3.4 μg/mL||Anticancer, compared with existed drugs. 79, 80|
|Human colon adenocarcinoma cell line COLO 320||200 μg/mL||Apoptosis, Bcl-2 gene expression 81, 82|
|24||Datura innoxia (Solanaceae)||Dinoxin B||Leaves||Human colon adenocarcinoma (HCT 15) and human larynx cancer cell lines (Hep-2)||300μg/ml||Decrease expression of antiapoptotic Bcl-2 protein 83, 84|
|Ethanolic extract||Bark||HeLa cell lines||191.5 μg/ml||cell cycle inhibition in G0/G1 phase 85, 86|
|Hypericin||Flower||MCF-7 cells, a human breast adenocarcinoma cell-line||0.5 (μg/ml)||Apoptosis 87, 88|
CONCLUSION: Medicinal plants are the source of bioactive compounds showing diverse functions on different biological systems. There are various plants mentioned in Ayurveda literature curing various diseases. Drugs currently available in the market induce various side effects and very costly. Most of the plant-derived products can be proved as cheap sources for drug formulation with reduced side effects. There are various phytocompounds used in curing cancer by the village folk, which have proved good in improving the survival rate of patients and boosting their immunity. However, there is a need to understand the molecular mechanism of action of these herbal formulations.
There is a great advancement in molecular science and structure determination techniques, so this review help researchers to use mentioned plants and perform various experimental studies on different cancer cell lines and test organisms. It will be helpful for pharmaceutical companies to use these active constituents to prepare drugs of anticancer drugs and understand their mechanism of action.
ACKNOWLEDGEMENT: I acknowledge the Head of Department (UIBT), Chandigarh University, Prof. Gunjan Mukharjee, and my departmental colleagues for giving me support to carry this work.
CONFLICTS OF INTEREST: The author report no conflicts of interest.
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How to cite this article:
Kumar A: The anticancer activity of bioactive compounds from medicinal plants: an review. Int J Pharm Sci & Res 2021; 12(8): 4115-21. doi: 10.13040/IJPSR.0975-8232.12(8).4115-21.
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