Apoptosis induction by an analog of curcumin (BDMC-A) in human laryngeal carcinoma cells through intrinsic and extrinsic pathways

Mohankumar, Kumaravel; Pajaniradje, Sankar; Sridharan, Subhashree; Singh, Vivek Kumar; Ronsard, Larance; Banerjea, Akhil C.; Selvanesan, Benson Chellakkan; Coumar, Mohane Selvaraj; Periyasamy, Latha; Rajagopalan, Rukkumani

doi:10.1007/s13402-014-0207-3

Cited by 25 publications

(12 citation statements)

References 51 publications

(47 reference statements)

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“…EGFR activates src and the overexpression of src increases the response of EGFRmediated processes. Previously, we showed that BDMC-A was more efficient in binding and inhibiting EGFR signals than curcumin [39]. That finding is consistent with the present finding that BDMC-A treatment reduces expression of src.…”

Section: Discussionsupporting

confidence: 93%

BDMC-A, an analog of curcumin, inhibits markers of invasion, angiogenesis, and metastasis in breast cancer cells via NF-κB pathway—A comparative study with curcumin

Mohankumar

Sridharan

Pajaniradje

et al. 2015

Biomedicine & Pharmacotherapy

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Section: Discussionsupporting

confidence: 93%

BDMC-A, an analog of curcumin, inhibits markers of invasion, angiogenesis, and metastasis in breast cancer cells via NF-κB pathway—A comparative study with curcumin

Mohankumar

Sridharan

Pajaniradje

et al. 2015

Biomedicine & Pharmacotherapy

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“…Changes in caspase-3 enzyme activity serve as important indicators of apoptosis [32]. These changes were examined using a caspase-3 colorimetric assay (BioVision Research Products; San Francisco, CA, USA).…”

Section: Caspase-3 Enzyme Activity Assaymentioning

confidence: 99%

“…During apoptotic cell death, phosphatidylserine (PS), a phospholipid component of the inner-leaflet of cell membranes [32], becomes available at the cell surface. This early marker of apoptotic cell death can be detected by staining with the green fluorescent dye Annexin V-FITC (BD Pharmingen, Germany).…”

Section: Phosphatidylserine Exposure and Cell Permeability Assaymentioning

confidence: 99%

Anti-proliferative, apoptotic and signal transduction effects of hesperidin in non-small cell lung cancer cells

et al. 2015

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Purpose Hesperidin, a glycoside flavonoid, is thought to act as an anti-cancer agent, since it has been found to exhibit both pro-apoptotic and anti-proliferative effects in several cancer cell types. The mechanisms underlying hesperidin-induced growth arrest and apoptosis are, however, not well understood. Here, we aimed to investigate the anti-proliferative and apoptotic effects of hesperidin on non-small cell lung cancer (NSCLC) cells and to investigate the mechanisms involved. Methods The anti-proliferative and apoptotic effects of hesperidin on two NSCLC-derived cell lines, A549 and NCI-H358, were determined using a WST-1 colorimetric assay, a LDH cytotoxicity assay, a Cell Death Detection assay, an AnnexinV-FITC assay, a caspase-3 assay and a JC-1 assay, respectively, all in a time-and dose-dependent manner. As a control, non-cancerous MRC-5 lung fibroblasts were included. Changes in whole genome gene expression profiles were assessed using an Illumina Human HT-12v4 beadchip microarray platform, and subsequent data analyses were performed using an Illumina Genome Studio and Ingenuity Pathway Analyser (IPA). Results We found that after hesperidin treatment, A549 and NCI-H358 cells exhibited decreasing cell proliferation and increasing caspase-3 and other apoptosis-related activities, in conjunction with decreasing mitochondrial membrane potential activities, in a dose-and time-dependent manner. Through a GO analysis, by which changes in gene expression profiles were compared, we found that the FGF and NF-κB signal transduction pathways were most significantly affected in the hesperidin treated NCI-H358 and A549 NSCLC cells. Conclusions Our results indicate that hesperidin elicits an in vitro growth inhibitory effect on NSCLC cells by modulating immune response-related pathways that affect apoptosis. When confirmed in vivo, hesperidin may serve as a novel antiproliferative agent for non-small cell lung cancer.

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“…Apoptosis is mediated by either an extrinsic pathway, triggered by extracellular stimuli, or by an intrinsic pathway, activated by intracellular modulators [20][21][22][23]. Mitochondria play a critical role in the intrinsic pathway by releasing a series of molecules, including cytochrome c. Within the cytosol, the binding of cytochrome c to adaptor protein Apaf-1 and pro-caspasse-9 molecules leads to the formation of the apoptosome that is responsible for activation of a caspase-dependent apoptotic pathway [24].…”

Section: Introductionmentioning

confidence: 99%

Anti-tumor effect of emodin on gynecological cancer cells

Wang

Zhang

et al. 2015

Cell Oncol.

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Apoptosis induction by an analog of curcumin (BDMC-A) in human laryngeal carcinoma cells through intrinsic and extrinsic pathways

Abstract: From our results we conclude that BDMC-A can induce apoptosis in Hep-2 laryngeal carcinoma cells more effectively than curcumin, and that this activity can be attributed to the presence of a hydroxyl group at the ortho position within this compound.

Cited by 25 publications

References 51 publications

BDMC-A, an analog of curcumin, inhibits markers of invasion, angiogenesis, and metastasis in breast cancer cells via NF-κB pathway—A comparative study with curcumin

BDMC-A, an analog of curcumin, inhibits markers of invasion, angiogenesis, and metastasis in breast cancer cells via NF-κB pathway—A comparative study with curcumin

Anti-proliferative, apoptotic and signal transduction effects of hesperidin in non-small cell lung cancer cells

Anti-tumor effect of emodin on gynecological cancer cells

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