Curcumin sensitizes human lung cancer cells to apoptosis and metastasis synergistically combined with carboplatin

Kang, Ji Ho; Kim, In Kyoung; Lee, Hwa Young; Ha, Jeonghoon; Yeo, Chang Dong; Kang, Hye Seon; Moon, Hwa Sik; Lee, Sang Haak

doi:10.1177/1535370215571881

Cited by 40 publications

(26 citation statements)

References 36 publications

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“…Curcumin has been suggested to induce cell cycle arrest and activate apoptosis-mediated cell death in several cancer cells, including lung cancer ( 7 – 9 ). Although it is strongly believed that apoptosis is the main toxic mechanism of curcumin in tumor cells, it is not completely known whether autophagy is induced in curcumin-caused cancer cell death.…”

Section: Introductionmentioning

confidence: 99%

Curcumin induced autophagy anticancer effects on human lung adenocarcinoma cell line A549

et al. 2017

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To investigate the anticancer effects of curcumin-induced autophagy and its effects on the human lung adenocarcinoma A549 cell line, inverted phase contrast microscopy was used to observe alterations to the cytomorphology of cells. An MTT assay was used to measure cell viability. Autophagy was detected using acridine orange (AO) staining and 3-methyladenine (3-MA) was used as an autophagy-specific inhibitor. Dose- and time-dependent A549 cell viability inhibition was observed following curcumin treatment. A dose-dependent increase in the red fluorescent structures in A549 cells was identified following curcumin treatment for 48 h through AO staining. In addition, the activation of autophagy was determined through changes in the number of autophagic vesicles (AVs; fluorescent particles) infected with monodansylcadaverine (MDC). The fluorescence intensity and density of AVs in the curcumin-treated groups were higher at 48 h compared with the control group. Finally, the MTT assay demonstrated that the survival rates of the curcumin-treated cells were increased when pretreated with 3-MA for 3 h, indicating that the inhibitory effect of curcumin on A549 cells is reduced following the inhibition of autophagy. Furthermore, AO and MDC staining confirmed that 3-MA does inhibit the induction of autophagy. Thus, it was hypothesized that the induction of autophagy is partially involved in the reduction of cell viability observed following curcumin treatment. The anticancer effects of curcumin on A549 cells can be reduced using autophagy inhibitors. This suggests a possible cancer therapeutic application of curcumin through the activation of autophagy. These findings have improved the understanding of the mechanism underlying the anticancer property of curcumin.

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Section: Introductionmentioning

confidence: 99%

Curcumin induced autophagy anticancer effects on human lung adenocarcinoma cell line A549

et al. 2017

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“…Therefore, for effective lung cancer treatment, efficient anti-metastatic and anti-angiogenic agents are required. Natural compounds have been shown to have enormous potential as anti-proliferative as well as anti-metastatic agents against multiple cancer types 1 2 3 4 5 . We have recently shown the strong anticancer potential of Cucurbitacin B (CuB) through epigenetic modulation against non-small cell lung cancer (NSCLC) in vitro as well as in vivo 6 .…”

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confidence: 99%

Cucurbitacin B inhibits the stemness and metastatic abilities of NSCLC via downregulation of canonical Wnt/β-catenin signaling axis

Shukla

Sinha

Khan

et al. 2016

Sci Rep

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Lack of effective anti-metastatic drugs creates a major hurdle for metastatic lung cancer therapy. For successful lung cancer treatment, there is a strong need of newer therapeutics with metastasis-inhibitory potential. In the present study, we determined the anti-metastatic and anti-angiogenic potential of a natural plant triterpenoid, Cucurbitacin B (CuB) against non-small cell lung cancer (NSCLC) both in vitro and in vivo. CuB demonstrated a strong anti-migratory and anti-invasive ability against metastatic NSCLC at nanomolar concentrations. CuB also showed significant tumor angiogenesis-inhibitory effects as evidenced by the inhibition of migratory, invasive and tube-forming capacities of human umbilical vein endothelial cells. CuB-mediated inhibition of angiogenesis was validated by the inhibition of pre-existing vasculature in chick embryo chorio-allantoic membrane and matrigel plugs. Similarly, CuB inhibited the migratory behavior of TGF-β1-induced experimental EMT model. The CuB-mediated inhibition of metastasis and angiogenesis was attributable to the downregulation of Wnt/β-catenin signaling axis, validated by siRNA-knockdown of Wnt3 and Wnt3a. The CuB-mediated downregulation of Wnt/β-catenin signaling was also validated using 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis model in vivo. Collectively, our findings suggest that CuB inhibited the metastatic abilities of NSCLC through the inhibition of Wnt/β-catenin signaling axis.

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“…It can be concluded from the results that combination of Ox with Cur is better in cell kill than that of lines (Montopoli, Ragazzi et al 2009). Moreover, curcumin and carboplatin in combination synergistically inhibited apoptosis and metastasis against lung cancer (Kang, Kang et al 2015).…”

Section: Discussionmentioning

confidence: 94%

Dose Dependent Synergism from Combination of Platinum Drugs with Curcumin Sgainst Colorectal Cancer Cell Lines

Bali¹,

Yu²,

Beale³

et al. 2020

J Angiotherapy

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Introduction: Colorectal cancer is the fourth most common cause of cancer mortality. More than 41265 new cases of colorectal cancer were detected and around 15903 colorectal cancer deaths occurred in year 2014 worldwide according to the statistical study from the cancer research. Chemotherapy is still in the main stream of the management of colorectal cancer along with surgery and radiotherapy. Aim: The objective of the present study was to investigate the activity of curcumin in combination with platinum drugs against colorectal cancer models (HT-29, Caco-2, LIM-1215 and LIM-2405). Methods: IC50 values of cisplatin (Cs), oxaliplatin (Ox), and curcumin (Cur) were determined against four human colorectal cancer cell lines using MTT reduction assay. Combined drug activity was determined as a factor of sequence of administration (0/0, 0/4 and 4/0 h) and added concentrations. DNA binding and proteomics were carried out to obtain insight into molecular mechanisms of drug action. Results: Oxaliplatin in combination with curcumin produced strong synergism in the tested cell lines. Cellular accumulation study, platinum-DNA binding study and DNA damage study revealed the mechanism of combined drug affects. Upregulation of K1C18, GRP78, IDHC and Cofilin-1 proteins was considered to be associated with the synergistic combined effects of Oxaliplatin with curcumin. Conclusion: Ox in combination Cur demonstrated very high synergism against HT-29 and Caco-2 cell lines. Synergism from Ox with Cur may be associated with greater platinum DNA binding. Proteomics revealed that the elevated expressions of K1C18, GRP78, IDHC and Cofilin1 may be responsible for the synergistic activity obtained from the combination of Ox with Cur.

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Curcumin sensitizes human lung cancer cells to apoptosis and metastasis synergistically combined with carboplatin

Cited by 40 publications

References 36 publications

Curcumin induced autophagy anticancer effects on human lung adenocarcinoma cell line A549

Curcumin induced autophagy anticancer effects on human lung adenocarcinoma cell line A549

Cucurbitacin B inhibits the stemness and metastatic abilities of NSCLC via downregulation of canonical Wnt/β-catenin signaling axis

Dose Dependent Synergism from Combination of Platinum Drugs with Curcumin Sgainst Colorectal Cancer Cell Lines

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