A novel synthetic curcumin derivative MHMM-41 induces ROS-mediated apoptosis and migration blocking of human lung cancer cells A549

Zhou, Guang‐Zhou; Li, Afang; Sun, Yan-He; Sun, Gang‐Chun

doi:10.1016/j.biopha.2018.04.086

Cited by 36 publications

(31 citation statements)

References 23 publications

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“…Moreover, ROS can also induce temporary or permanent cell cycle arrest, and act as signaling molecules that lead to enhanced cytotoxicity and apoptosis by increasing oxidative stress (47,48). Thus, intracellular ROS levels have become a key indicator for a number of chemotherapeutic agents in the induction of cancer cell apoptosis (49)(50)(51). In the present study, andrographolide significantly increased the intracellular levels of ROS.…”

Section: Discussionsupporting

confidence: 47%

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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Section: Discussionsupporting

confidence: 47%

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

Wang

Chen

et al. 2020

Int J Oncol

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“…Non-small lung cancer (NSCLC) constitutes 80–85% of total lung cancer, with a characteristic of slow cell division and relatively late metastasis. 1 , 2 Currently, surgical resection, adjuvant radio chemotherapy, molecular targeted therapy and immunotherapy have made great development these years, the 5-year overall survival rate of patients with lung cancer is only about 10–20%. 3 – 5 Cisplatin (DDP) is a first-line chemotherapy of NSCLC and chemoresistance of DDP seriously leads to poor prognosis of patients.…”

Section: Introductionmentioning

confidence: 99%

<p>Exosome-Reversed Chemoresistance to Cisplatin in Non-Small Lung Cancer Through Transferring miR-613</p>

Li¹,

Meng²,

Niu³

2020

CMAR

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Introduction: Non-small lung cancer (NSCLC) is one of the most common malignant tumors in the world. Chemoresistance is the main reason of adverse effects leading to the death of patients; thus, it is important to discover the potential target of chemotherapeutic resistance. Methods: The expression of differentially expressed miRNA was detected in BEAS-2B, A549 and A549/cisplatin (DDP) by qRT-PCR. Transmission electron microscopy (TEM) and exosome biomarkers were used to validate the extracted exosome. Cells incubated with miR-613 enriched exosomes were used to detect the function of exo-miR-613 in vitro. Then, exo-miR-613 was injected to mice treated with DDP to investigate the function role of exo-miR-613 in vivo. Results: Comparing to BEAS-2B, the expression of miR-613 inA549 was significantly reduced, which was more obvious in A549/DDP. After incubated with exo-miR-613 and corresponding exo-negative control (NC), we found overexpression of miR-613 remarkably increased the inhibition of cell proliferation induced by cisplatin. Exo-miR-613 fused into cells to significantly enhance the inhibited effect of DDP on the proliferation, migration and showed a promotion on cell apoptosis and DNA damage. The in vivo study showed that exo-miR-613 significantly inhibited the tumor growth, and promote the sensitivity to DDP, probably by down-regulating the expressions of GJA1, TBP and EIF-4E in tumor cells and tissues. Conclusion: Exo-miR-613 reversed chemoresistance to DDP in NSCLC cell to involve in the process of tumor progression, and might be a potential therapeutic strategy for NSCLC.

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“…Previous studies indicated that ROS has a critical role in anticancer drug-mediated apoptosis (26,27). Therefore, the effects of ALT and GEM on ROS production in A549 and NCI-H520 cells were assessed by flow cytometry.…”

Section: Resultsmentioning

confidence: 99%

Alantolactone enhances gemcitabine sensitivity of lung cancer cells through the reactive oxygen species-mediated endoplasmic reticulum stress and Akt/GSK3β pathway

et al. 2019

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Lung cancer is one of the leading causes of cancer-associated mortality in china and globally. Gemcitabine (GEM), as a first-line therapeutic drug, has been used to treat lung cancer, but GEM resistance poses a major limitation on the efficacy of GEM chemotherapy. Alantolactone (ALT), a sesquiterpene lactone compound isolated from Inula helenium, has been identified to exert anticancer activity in various types of cancer, including breast, pancreatic, lung squamous and colorectal cancer. However, the underlying mechanisms of the anticancer activity of ALT in lung cancer remain to be fully elucidated. The present study aimed to determine whether ALT enhances the anticancer efficacy of GEM in lung cancer cells and investigated the underlying mechanisms. The cell viability was assessed with a cell counting Kit-8 assay. The cell cycle, apoptosis and the level of reactive oxygen species (ROS) were assessed by flow cytometry, and the expression of cell cycle-associated and apoptosis-associated proteins were determined by western blot analysis. The results demonstrated that ALT inhibited cell growth and induced S-phase arrest and cell apoptosis in A549 and NcI-H520 cells. Furthermore, ALT increased the level of ROS, inhibited the Akt/glycogen synthase kinase (GSK)3β pathway and induced endoplasmic reticulum (ER) stress in A549 and NcI-H520 cells. Additionally, ALT treatment sensitized lung cancer cells to GEM. Analysis of the molecular mechanisms further revealed that ALT enhanced the anticancer effects of GEM via ROS-mediated activation of the Akt/GSK3β and ER stress pathways. In conclusion, combined treatment with ALT and GEM may have potential as a clinical strategy for lung cancer treatment.

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A novel synthetic curcumin derivative MHMM-41 induces ROS-mediated apoptosis and migration blocking of human lung cancer cells A549

Cited by 36 publications

References 23 publications

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

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

<p>Exosome-Reversed Chemoresistance to Cisplatin in Non-Small Lung Cancer Through Transferring miR-613</p>

Alantolactone enhances gemcitabine sensitivity of lung cancer cells through the reactive oxygen species-mediated endoplasmic reticulum stress and Akt/GSK3β pathway

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