Activation of AIFM2 enhances apoptosis of human lung cancer cells undergoing toxicological stress

Lü, Jun; Chen, Jian; Xu, Nianjun; Wu, Jun; Kang, Yani; Shen, Tingting; Kong, Hualei; Ma, Chi; Cheng, Ming; Shao, Zongshu; Xu, Ling; Zhao, Xiaodong

doi:10.1016/j.toxlet.2016.07.002

Cited by 37 publications

(46 citation statements)

References 28 publications

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“…Apoptosis-inducing factor, mitochondrion-associated 2 (AIFM2), a homologue of AIF, have been proved to induce apoptosis in cancers. For example, activated AIFM2 enhanced apoptosis of human lung cancer cells undergoing toxicological stress (25). Down-regulated expression of AIFM2 was detected in various cancers, including in pediatric acute myeloid leukemia, indicating an anticancer effect (26,27).…”

Section: The Inhibitory Effect Of Meg3/mir-214/aifm2 Axis On the Growmentioning

confidence: 99%

The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma

Fan

Deng

et al. 2017

International Journal of Oncology

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T-cell lymphoblastic lymphoma (T-LBL) is an aggressive malignancy with poor prognosis and high recurrence rate. Long non-coding RNA (lncRNA)-MEG3 is an important tumor suppressor in various cancers. The present study investigated the potential role of maternally expressed gene 3 (MEG3) in the progression of T-LBL. Suppressed expression of MEG3 was detected in T-LBL tissues compared with adjacent histologically normal tissues. Down-regulated level of MEG3 was also found in three T-LBL cell lines (CCRF-CEM, Jurkat and SUP-T1) compared with human T-cell line H9. The proliferation of T-LBL cells was inhibited and cell apoptosis rate was largely promoted when MEG3 was upregulated by a lentiviral vector. Further research revealed that microRNA (miRNA)-214 is a direct target of MEG3. The expression of miR-214 was increased in T-LBL tissues and cell lines compared with control groups. Besides, decreased level of miR-214 was elevated adding miR-214 mimic in SUP-T1 cells transfected with LncRNA-MEG3. Similarly, upregulated level of miR-214 was downregulated adding miR-214 inhibitor in SUP-T1 cells transfected with MEG3 siRNA. Luciferase activity assay further confirmed the targeting relationship between MEG3 and miR-214. Moreover, AIFM2 protein was predicted as a target of miR-214. The expression of AIFM2 was increased by MEG3 and was downregulated by miR-214 mimic. miRNA-214 reversed the effect of MEG3 on inhibiting cell proliferation and inducing cell apoptosis and cell cycle arrest in SUP-T1 cells. Moreover, relative expression of AIFM2 had a positive correlation with the expression of MEG3 and was negatively affected by miR-214. In vivo, MEG3 effectively suppressed tumor growth and the expression of proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA). Taken together, our research revealed that MEG3 worked as an anti-oncogene in T-LBL, and the MEG3-miR-214-AIFM2 pathway regulated the growth of T-LBL, providing potential prognosis markers as well as new potential targets for T-LBL treatment.

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Section: The Inhibitory Effect Of Meg3/mir-214/aifm2 Axis On the Growmentioning

confidence: 99%

The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma

Fan

Deng

et al. 2017

International Journal of Oncology

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“…YYJD is a new formula optimized from our previously published Jinfukang 8–10, 13 using Placket-Burman and random forests algorithm 12 . The half maximal inhibitory concentration (IC50) of YYJD and Jinfukang were 70 µg/ml and 570 µg/ml respectively in A549 cell, and 50 µg/ml and 640 µg/ml respectively in 95-D cell, determined by CCK8 cell viability assay.…”

Section: Resultsmentioning

confidence: 99%

“…Jinfukang is a herb formula and has been clinically used to treat human lung cancer patients for many years. Previous studies have revealed that Jinfukang inhibits tumor growth in mice model of lung cancer, suppresses cellular proliferation and induces apoptosis of lung cancer cells 8–10 . However, the twelve herbs in the formula make it difficult to elucidate the anti-tumor mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Herbal formula YYJD inhibits tumor growth by inducing cell cycle arrest and senescence in lung cancer

Zheng

Que

Jiao

et al. 2017

Sci Rep

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Lung cancer represents a major cause of cancer-related death worldwide. Although various tactics and anti-tumor drugs have been used to improve curative effects, five-year survival rate of lung cancer patients remains poor. In this study, we investigated the action and underlying mechanisms of our recently optimized Chinese herbal formula Yangyinjiedu (YYJD) against lung cancer. YYJD significantly inhibits the proliferation of lung cancer cell lines (95-D, A549, H460 and H1975) by inducing cell cycle arrest and senescence in a dose-dependent manner. In particular, YYJD induces significant G2/M phase arrest and inhibits the colony formation of lung cancer cells. Moreover, we found that administration of YYJD could inhibit the growth of xenografted lung cancer cells in nude mice without loss in body weight. Our findings suggest that the herbal formula YYJD is a potential anti-tumor agent against lung cancer.

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“…Transcription level of genes of interest was evaluated using quantitative reverse transcription-quantitative polymerase chain reaction (RT-qPCR) with SYBR-Green PCR Master Mix (Qiagen). RT-qPCR was performed according to our previous studies ( 13 , 16 , 17 ). All primer sequences used for RT-qPCR are presented in Table II .…”

Section: Methodsmentioning

confidence: 99%

“…As the majority of TCMs consist of various components, it is necessary to utilize high-throughput strategies to delineate the underlying mechanisms ( 11 ). Previous studies have shown that cDNA profiling may be effectively used to characterize the antitumor mechanism by measuring gene expression changes ( 12 , 13 ). With the emergence of RNA-seq, this approach has provided a better platform to investigate the mechanisms of various drugs due to its performance in robustness and effectiveness ( 14 , 15 ).…”

Section: Introductionmentioning

confidence: 99%

Jinfukang induces cellular apoptosis through activation of Fas and DR4 in A549 cells

et al. 2018

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The traditional Chinese medicine Jinfukang (JFK) has been shown as a valuable drug to treat non-small cell lung cancer (NSCLC). Previously, it was reported that JFK-induced epigenetic alteration is involved in anti-lung cancer activity. In the present study, the effect of JFK on lung cancer cell lines was examined with the aim to further understand the underlying mechanisms of JFK-induced anti-lung cancer activity by transcriptome profiling analysis. JFK was observed to decrease lung cancer cell viability and simultaneously induce cellular morphology alteration. Additionally, this causes cell cycle arrest and apoptosis in A549 cells. The present RNA-seq analysis identified 5,281 genes with differential expression (P<0.05). Gene ontology analysis indicated that genes involved in the cell cycle pathway are downregulated, including cyclin-dependent kinase 2, cyclin-dependent kinase 4, cyclin B1 and cyclin A2, and apoptosis-associated genes are upregulated, including Fas, death receptor 4 (DR4), tumor protein P53 binding protein 2 and BCL2 interacting protein 3 like. Particularly, the present results indicate knockdown of Fas and DR4 attenuates JFK-induced apoptosis in A549 cells. Overall, the present study suggests JFK induces cellular apoptosis through activation of Fas and DR4 in A549 cells and provides an insight for understanding the antitumor mechanisms of this Chinese traditional medicine.

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Activation of AIFM2 enhances apoptosis of human lung cancer cells undergoing toxicological stress

Cited by 37 publications

References 28 publications

The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma

The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma

Herbal formula YYJD inhibits tumor growth by inducing cell cycle arrest and senescence in lung cancer

Jinfukang induces cellular apoptosis through activation of Fas and DR4 in A549 cells

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