Andrographolide Suppresses Proliferation of Nasopharyngeal Carcinoma Cells via Attenuating NF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold-italic">κ</mml:mi></mml:mrow></mml:math>B Pathway

Peng, Tao; Hu, Min; Wu, Tingting; Zhang, Cen; Chen, Zhe; Huang, Shuo; Zhou, Xuhong

doi:10.1155/2015/735056

Cited by 27 publications

(24 citation statements)

References 20 publications

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“…Previous study has reported NF-κB inhibitors DHMEQ and BAY 11-7082, by blocking the nuclear translocation of activated NF-κB were effective in inhibiting NPC HK1 cell growth, induced apoptosis and abrogated their invasiveness and anchorage independent growth104. Furthermore, recent study by Peng et al 105. also showed that andrographolide inhibited proliferation and invasiveness of NPC HK1 cells via suppressing NF-κB transcriptional activity, thus providing a rational for the possibility of utilizing the NF-κB activation status to stratify NPC patients who may be more likely to benefit therapy with NF-κB inhibitors.…”

Section: Discussionmentioning

confidence: 94%

Exome Sequencing Identifies Potentially Druggable Mutations in Nasopharyngeal Carcinoma

Chow

Tan

Chai

et al. 2017

Sci Rep

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In this study, we first performed whole exome sequencing of DNA from 10 untreated and clinically annotated fresh frozen nasopharyngeal carcinoma (NPC) biopsies and matched bloods to identify somatically mutated genes that may be amenable to targeted therapeutic strategies. We identified a total of 323 mutations which were either non-synonymous (n = 238) or synonymous (n = 85). Furthermore, our analysis revealed genes in key cancer pathways (DNA repair, cell cycle regulation, apoptosis, immune response, lipid signaling) were mutated, of which those in the lipid-signaling pathway were the most enriched. We next extended our analysis on a prioritized sub-set of 37 mutated genes plus top 5 mutated cancer genes listed in COSMIC using a custom designed HaloPlex target enrichment panel with an additional 88 NPC samples. Our analysis identified 160 additional non-synonymous mutations in 37/42 genes in 66/88 samples. Of these, 99/160 mutations within potentially druggable pathways were further selected for validation. Sanger sequencing revealed that 77/99 variants were true positives, giving an accuracy of 78%. Taken together, our study indicated that ~72% (n = 71/98) of NPC samples harbored mutations in one of the four cancer pathways (EGFR-PI3K-Akt-mTOR, NOTCH, NF-κB, DNA repair) which may be potentially useful as predictive biomarkers of response to matched targeted therapies.

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Section: Discussionmentioning

confidence: 94%

Exome Sequencing Identifies Potentially Druggable Mutations in Nasopharyngeal Carcinoma

Chow

Tan

Chai

et al. 2017

Sci Rep

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“…In the present study, treatment with 20 µM andrographolide significantly attenuated the protein expression of NF-κB-p65 in SW620 cells. Peng et al also reported that andrographolide suppresses NF-κB expression in nasopharyngeal carcinoma cells (26).…”

Section: Discussionmentioning

confidence: 98%

Andrographolide suppresses proliferation of human colon cancer SW620 cells through the TLR4/NF-κB/MMP-9 signaling pathway

Zhang

Zhao

et al. 2017

Oncology Letters

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Abstract. Modern pharmacological research has revealed that andrographolide has various functions, including anti-bacterial, anti-inflammatory and anti-viral effects, immunoregulation, treating cardiovascular and cerebrovascular diseases, and prevention and treatment of alcoholic liver injury. The present study investigated whether andrographolide suppresses the proliferation of human colon cancer cell through the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB/matrix metalloproteinase-9 (MMP-9) signaling pathway. The MTT assay and lactate dehydrogenase assay were used to evaluate the anticancer effects of andrographolide on cell proliferation and cytotoxicity in human colon cancer SW620 cells.Flow cytometry was used to analyze the anticancer effects of andrographolide on apoptosis by Annexin V-fluorescein isothiocyanate/propidium iodide kit. The effects of andrographolide on the activity of caspase-3/9 were measured using ELISA. Western blot analysis was also used to analyze the protein expression of TLR4, myeloid differentiation primary response gene 88 (MyD88), NF-κB-p65 and MMP-9. In the present study, it was found that andrographolide suppressed the cell proliferation, augmented cytotoxicity, evoked cell apoptosis and activated caspase-3/9 activities in human colon cancer SW620 cells. The results revealed that the anti-proliferation effects of andrographolide on the SW620 cells was associated with the inhibition of TLR4, MyD88, NF-κB-p65 and MMP-9 signaling activation. The results suggest that andrographolide is a promising drug for treatment of human colon cancer via suppression of the TLR4/NF-κB/MMP-9 signaling pathway.

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“…Thus, novel treatments are required to improve the outcomes of patients with osteosarcoma. Andrographolide has been reported to be a promising therapeutic for treatment of multiple types of cancer, with potent antitumor effects and minimal toxicity (11,29,(39)(40)(41)(42). However, little is known about the effects and biochemical mechanisms of action of andrographolide in osteosarcoma.…”

Section: Discussionmentioning

confidence: 99%

Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway

Wang

Chen

et al. 2020

Int J Oncol

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Osteosarcoma is the most common primary malignant tumor of the bone and the long-term survival of patients with this disease has remained unsatisfactory over the past several decades. Andrographolide, a traditional drug used in Chinese medicine, has been found to exert a significant antitumor effect against several types of cancer. However, relatively little is known about the effect of andrographolide on osteosarcoma and the underlying mechanisms. In the present study, it was shown that andrographolide inhibited osteosarcoma cell proliferation by arresting the cell cycle at the G2/M phase and increasing caspase-mediated apoptosis. Furthermore, treatment with andrographolide induced JNK activation and increased production of reactive oxygen species (ROS). The andrographolide-triggered apoptosis in osteosarcoma cells was partly abrogated by a JNK inhibitor and completely reversed by a ROS scavenger. Additionally, JNK activation and cell cycle arrest at the G2/M phase were prevented by administration of an ROS scavenger. In vivo, it was also found that andrographolide inhibited tumor growth by increasing the levels of ROS and activating JNK; thus inducing cytotoxicity in primary osteosarcoma cells. Together, the results of the present study suggest that andrographolide caused G2/M arrest and induced cell apoptosis via regulation of the ROS/JNK signaling pathway in osteosarcoma cells. Thus, andrographolide may serve as a promising antitumor therapeutic agent against osteosarcoma.

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Andrographolide Suppresses Proliferation of Nasopharyngeal Carcinoma Cells via Attenuating NF-κB Pathway

Cited by 27 publications

References 20 publications

Exome Sequencing Identifies Potentially Druggable Mutations in Nasopharyngeal Carcinoma

Exome Sequencing Identifies Potentially Druggable Mutations in Nasopharyngeal Carcinoma

Andrographolide suppresses proliferation of human colon cancer SW620 cells through the TLR4/NF-κB/MMP-9 signaling pathway

Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway

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