Natural compounds as potential adjuvants to cancer therapy: Preclinical evidence

Lin, Shian-Ren; Hsu, Che-Fang; Tsai, May Jwan; Cheng, Henrich; Leong, Max K.; Sung, Ping Jyun; Chen, Jian Chyi; Weng, Ching‐Feng

doi:10.1111/bph.14816

Cited by 286 publications

(211 citation statements)

References 104 publications

(113 reference statements)

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“…Furthermore, in recent decades, a significant number of medicinal herbs have been reported to have biofunctional effects in treating chronic liver diseases through eliminating viruses, alleviating fibrogenesis, and suppressing tumorigenesis. As a result, plant extracts can be considered as potential anti-cancer candidates for cancer therapy [ 9 , 10 ]. Here, in the first study to investigate the anti-hepatoma activity of CAt extract in vitro and in vivo, our results first found that HCC cells were inhibited by CAt extract; nevertheless, the cytotoxicity of CAt extract was moderate against normal cells, including liver embryonic cells, kidney epithelial cells, and endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…The genus Cedrus contains at least four species: C. deodara , C. libani , C. brevifolia , and C. atlantica . Among these, C. deodara is widely studied in regard to different biofunctions, such as anti-inflammatory [ 10 ], anti-cancer [ 11 , 12 , 13 , 14 , 15 , 16 ], anti-oxidant [ 17 ], and antimicrobial activities [ 18 , 19 ]. In terms of its anti-cancer activity, it has been shown that C. deodara extract has obvious inhibitory effects on tumor growth in various cancers such as leukemia.…”

Section: Introductionmentioning

confidence: 99%

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Extract Derived from Cedrus atlantica Acts as an Antitumor Agent on Hepatocellular Carcinoma Growth In Vitro and In Vivo

et al. 2020

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Cedrus atlantica is widely used in herbal medicine. However, the anti-cancer activity of C. atlantica extract (CAt extract) has not been clarified in hepatocellular carcinoma. In the study, we elucidated the anti-hepatoma capacity of CAt extract on HCC in vitro and in vivo. To explore the anti-hepatoma mechanisms of the CAt extract in vitro, HCC and normal cells were treated with the CAt extract, which showed marked inhibitory effects on HCC cells in a dose-dependent manner; in contrast, the CAt extract treatment was less cytotoxic to normal cells. In addition, our results indicate that the CAt extract induced apoptosis via caspase-dependent and independent apoptosis pathways. Furthermore, the CAt extract inhibited HCC tumor cell growth by restraining cell cycle progression, and it reduced the signaling of the AKT, ERK1/2, and p38 pathways. In the xenograft model, the CAt extract suppressed HCC tumor cell growth and prolonged lifespan by inhibiting PCNA protein expression, repressing part of the VEGF-induced autocrine pathway, and triggering strong expression of cleaved caspase-3, which contributed to cell apoptosis. Moreover, the CAt extract did not induce any obvious changes in pathological morphology or body weight, suggesting it had no toxicity. CAt extract exerted anti-tumor effects on HCC in vitro and in vivo. Thus, CAt extract could be used as a potential anti-cancer therapeutic agent against HCC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Extract Derived from Cedrus atlantica Acts as an Antitumor Agent on Hepatocellular Carcinoma Growth In Vitro and In Vivo

et al. 2020

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“…These observations indicate that CA may inhibit growth and induce apoptosis in these aggressive cells which are prone to acquiring drug resistance. Recent studies have demonstrated that drug combinations are much more effective in cancer treatment than single molecules, with many advantages, such as reduced emergence of drug resistance being utmost important, along with increased patient survival (Lin et al, 2019; Lodi et al, 2017) and the obvious economic benefits (Karlsson, Nygren, & Glimelius, 2001; Mokhtari et al, 2017). Our finding showing growth‐inhibitory and apoptosis promoting ability of CA in TNBCs may result in additional benefits if used in combination therapy regimens.…”

Section: Discussionmentioning

confidence: 99%

Chebulinic acid inhibits MDA‐MB‐231 breast cancer metastasis and promotes cell death through down regulation of SOD1 and induction of autophagy

Sharma

Mishra

Thacker

et al. 2020

Cell Biology International

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Triple‐negative breast cancers (TNBC) are highly aggressive and drug resistant accounting for majority of cases with poor outcome. Purified natural compounds display substantial anticancer activity with reduced cytotoxicity providing a new avenue to combat TNBC. Chebulinic acid (CA), a polyphenol derived from the fruits of various medicinal plants has potent anticancer activity. Here, we demonstrate that CA shows significant cytotoxicity against triple negative MDA‐MB‐231 cells. CA exhibited cytotoxicity to MDA‐MB‐231 cells in 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. Further, CA mitigated MDA‐MB‐231 cells viability and proliferation as shown by reduced live cell count, crystal violet staining, colony formation assay, soft agar assay and cell cycle analysis. Wound healing assay and trans‐well migration assay demonstrated that CA significantly inhibited migration of MDA‐MB‐231 cells. Also reduced MMP9 expression was observed in CA‐treated cells by gelatin zymography. CA negatively regulated mesenchymal characteristics of MDA‐MB‐231 cells demonstrated by F‐actin staining and reduced expression of N‐cadherin by confocal microscopy and western blot analysis. Annexin V/propidium iodide (PI) and active caspase‐3 staining showed that CA was able to induce apoptosis in MDA‐MB‐231 cells but did not activate caspase‐3. Two‐dimensional gel electrophoresis based proteomic analysis demonstrated that CA regulated proteins belonging to the oxidative stress pathway, apoptotic pathway and proteins with antiproliferative activity. Western blot analysis analysis revealed that CA negatively regulated superoxide dismutase 1 (SOD1) and enhanced oxidative stress in MDA‐MB‐231 cells. SOD1 in‐gel activity assay also showed reduced SOD1 activity upon CA treatment. Overexpression studies with GFP‐LC3 and tandem tagged RFP‐GFP‐LC‐3 also demonstrated enhanced autophagy upon CA treatment.

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“…Recently, the use of selective, potent, and relatively non-toxic natural compounds to impede tumors and enhance chemosensitivity has gained immense importance [19]. Moreover, some natural plant products exhibit excellent in inhibiting Wnt/β-catenin signaling and improving chemosensitivity in some cancers [20].…”

Section: Introductionmentioning

confidence: 99%

Cardamonin Enhances Cisplatin Chemosensitivity of Nasopharyngeal Cancer Cells via Attenuating c-Myc-Mediated β-Catenin/ABCG2 Signaling

Qiao¹,

Li²,

Wu³

et al. 2020

Preprint

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Purpose: Resistance to chemotherapeutic drugs in nasopharyngeal carcinoma(NPC) remains a major obstacle of clinical therapy. To address the issue, screening for natural low-toxicity products as chemosensitizers has become a promising strategy for cancer therapy. In this study, we investigated chemosensitizing effects of cardamonin (CM), a plant-derived chalcone, on cisplatin (DPP)-resistant NPC cells, and explored the molecular mechanism for its antitumor activity. Methods: The chemotherapeutic efficacy of cardamonin, cisplatin and their combination in cisplatin-resistant NPC cells were analyzed using MTT assay, apoptosis assay, and cell cycle analysis. Real-time PCR, western blotting, and cell transfection analysis were performed to assess the synergistic inhibitory action of cardamonin supplemented with cisplatin on Wnt/β-catenin/ABCG2 signaling. The effect of cardamonin on ABCG2 drug efflux function was analyzed by doxorubicin accumulation assay. A CNE2/DPP nude mouse model was used to determine the combinatorial effects of cardamonin on tumor growth in vivo. Results: Cardamonin increased cisplatin-induced cytotoxicity, accompanied by induction of apoptosis and cell cycle arrest in DPP-resistant NPC cells. Moreover, cardamonin could synergized with cisplatin to downregulate β-catenin, c-Myc, and ABCG2. Specifically, cardamonin inhibited Wnt/β-catenin/ABCG2 signaling through c-Myc-mediated transcription inactivation, thereby suppressing the expression of ABCG2 in cisplatin-resistant NPC cells. These findings were confirmed in vivo, wherein cardamonin treatment with cisplatin resulted in reduced tumor growth in a CNE2/DPP xenograft animal model. Conclusions: Taken together, our data firstly demonstrated that cardamonin increased chemosensitivity of nasopharyngeal cancer cells to cisplatin through inactivation of Wnt/β-catenin/ABCG2 signaling, more specifically by inhibition of β-catenin/ABCG2 signaling through c-Myc-mediated transcriptional inactivation, thereby downregulation of ABCG2 and reversal of cisplatin resistance. Thus, in addition to its chemotherapeutic potential, cardamonin may serve as a useful chemosensitizer to conventional chemotherapeutic drugs in the treatment of nasopharyngeal carcinoma.

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Natural compounds as potential adjuvants to cancer therapy: Preclinical evidence

Cited by 286 publications

References 104 publications

Extract Derived from Cedrus atlantica Acts as an Antitumor Agent on Hepatocellular Carcinoma Growth In Vitro and In Vivo

Extract Derived from Cedrus atlantica Acts as an Antitumor Agent on Hepatocellular Carcinoma Growth In Vitro and In Vivo

Chebulinic acid inhibits MDA‐MB‐231 breast cancer metastasis and promotes cell death through down regulation of SOD1 and induction of autophagy

Cardamonin Enhances Cisplatin Chemosensitivity of Nasopharyngeal Cancer Cells via Attenuating c-Myc-Mediated β-Catenin/ABCG2 Signaling

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