Knockdown of hepatoma-derived growth factor-related protein-3 induces apoptosis of H1299 cells via ROS-dependent and p53-independent NF-κB activation

Yun, Hong Shik; Baek, Jeong‐Hwa; Yim, Ji-Hye; Lee, Su‐Jae; Lee, Chang-Woo; Song, Jie‐Young; Um, Hong‐Duck; Park, Jong Kuk; Park, In-Chul; Hwang, Sang‐Gu

doi:10.1016/j.bbrc.2014.05.039

Cited by 12 publications

(12 citation statements)

References 17 publications

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“…It regulates the transcription of DNA, and mediates apoptosis in response to oxidative stress [38]. Recent studies have demonstrated that ROS-dependent NF-kB activation induced the protein expression of c-Myc and Noxa in p53-independent human NSCLC cell death [50]. On the contrary, NF-kB activation was involved in resistance to oxidative stress and p53-mediated programmed cell death [51–53].…”

Section: Discussionmentioning

confidence: 99%

Artocarpin, an isoprenyl flavonoid, induces p53-dependent or independent apoptosis via ROS-mediated MAPKs and Akt activation in non-small cell lung cancer cells

Tsai

Liu²,

Chiang

et al. 2017

Oncotarget

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Artocarpin has been shown to exhibit cytotoxic effects on different cancer cells, including non-small cell lung carcinoma (NSCLC, A549). However, the underlying mechanisms remain unclear. Here, we explore both p53-dependent and independent apoptosis pathways in artocarpin-treated NSCLC cells. Our results showed that artocarpin rapidly induced activation of cellular protein kinases including Erk1/2, p38 and AktS473. Inhibition of these protein kinases prevented artocarpin-induced cell death. Moreover, artocarpin-induced phosphorylation of these protein kinases and apoptosis were mediated by induction of reactive oxygen species (ROS), as pretreatment with NAC (a ROS scavenger) and Apocynin (a Nox-2 inhibitor) blocked these events. Similarly, transient transfection of p47Phox or p91Phox siRNA attenuated artocarpin-induced NADPH oxidase activity and cell death. In addition, p53 dependent apoptotic proteins including PUMA, cytochrome c, Apaf-1 and caspase 3 were activated by artocarpin, and these effects can be abolished by antioxidants, MAPK inhibitors (U0126 and SB202190), but not by PI3K inhibitor (LY294002). Furthermore, we found that artocarpin-induced Akt phosphorylation led to increased NF-κB activity, which may act as an upstream regulator in the c-Myc and Noxa pathway. Therefore, we propose that enhancement of both ERK/ p38/ p53-dependent or independent AktS473/NF-κB/c-Myc/Noxa cascade by Nox-derived ROS generation plays an important role in artocarpin-induced apoptosis in NSCLC cells.

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Section: Discussionmentioning

confidence: 99%

Artocarpin, an isoprenyl flavonoid, induces p53-dependent or independent apoptosis via ROS-mediated MAPKs and Akt activation in non-small cell lung cancer cells

Tsai

Liu²,

Chiang

et al. 2017

Oncotarget

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“…For example, hepatoma‐derived growth factor‐related protein‐3, which has an anti‐apoptotic effect (Yun et al . ), was increased to 143.9% in the AMY (Fig. c).…”

Section: Resultsmentioning

confidence: 84%

“…There were also some protective factors activated after OVX. For example, hepatomaderived growth factor-related protein-3, which has an anti-apoptotic effect (Yun et al 2014), was increased to 143.9% in the AMY (Fig. 3c).…”

Section: Resultsmentioning

confidence: 95%

Evidence of altered depression and dementia‐related proteins in the brains of young rats after ovariectomy

Fang

Zeng

et al. 2018

Journal of Neurochemistry

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Menopause, a risk factor for brain dysfunction in women, is characterized by neuropsychological symptoms including depression and dementia, which are closely related to alterations in different brain regions after menopause. However, little is known about the variability in pathophysiologic changes associated with menopause in the brain. Here, we observed that menopause in rats induced by bilateral ovariectomy (OVX) showed depressive and dementia-related behaviors along with neuronal loss in the prefrontal cortex (PFC), hippocampus (HIP), hypothalamus (HYP), and amygdala (AMY) by Nissl staining. Meanwhile, by immunohistochemical staining, increased microglia in the HIP and AMY and increased astrocytes in the PFC, HYP, and AMY were shown. Using quantitative proteomics, we identified 146 differentially expressed proteins in the brains of OVX rats, for example, 20 in the PFC, 41 in the HIP, 17 in the HYP, and 79 in the AMY, and performed further detection by western blotting. A link between neuronal loss and apoptosis was suggested, as evidenced by increases in adenylate kinase 2 (AK2), B-cell lymphoma 2 associated X (Bax), cleaved caspase 3, and phosphorylated p53 and decreases in Huntingtin-interacting protein K, hexokinase, and phosphorylated B-cell lymphoma 2 (Bcl-2), and apoptosis might be triggered by endoplasmic reticulum stress (probed by increased glucose-regulated protein 78 (GRP78), cleaved caspase 12, phosphorylated protein kinase R (PKR)-like endoplasmic reticulum kinase, inositol-requiring enzyme-1 and activating transcription factor 6), and mitochondrial dysfunction (probed by increased cytochrome c and cleaved caspase 3 and decreased sideroflexin-1 (SFXN1) and NADH dehydrogenase (ubiquinone) 1 α subcomplex 11 (NDUFA11)). Activation of autophagy was also indicated by increased autophagy-related 7, γ-aminobutyric acid (GABA) receptor-associated protein-like 2, and oxysterol-binding protein-related protein 1 and confirmed by increased microtubule-associated protein light chain 3 (LC3II/I), autophagy-related 5, and Beclin1 in the HIP and AMY. In the AMY, which is important in emotion, higher GABA transporter 3 and lower vesicular glutamate transporter 1 levels indicated an imbalance between excitatory and inhibitory neurotransmission, and the increased calretinin and decreased calbindin levels suggested an adjustment of GABAergic transmission after OVX. In addition, cytoskeletal abnormalities including tau hyperphosphorylation, dysregulated Ca² signals, and glutamic synaptic impairments were observed in the brains of OVX rats. Collectively, our study showed the changes in different brain regions related to depression and dementia during menopause.

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“…Drug resistance of lung cancer cells is mainly attributed to resistance to apoptotic cell death. Induction of apoptotic cell death is the main mechanism of action of agents used for the treatment of lung cancer (16). The redox status of cells may determine their viability.…”

Section: Discussionmentioning

confidence: 99%

Miltirone‑induced apoptosis in cisplatin‑resistant lung cancer cells through upregulation of p53 signaling pathways

Zhu

2018

Oncol Lett

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The active ingredients of natural plants are important sources of antitumor agents. Miltirone is a major effective ingredient in traditional Chinese medicine and it is considered to have anti-infection and immunosuppressive activities. Clinically, it is often used for the treatment of arthritis and immune diseases. The effect of miltirone on cisplatin-resistant lung cancer cells has not been investigated to date. The present study aimed to examine the anticancer effect of miltirone in cisplatin-resistant lung cancer cells. Treatment with miltirone suppressed cell viability and induced apoptosis in HCC827 and A549 platinum-resistant lung cancer cells. It was also revealed that miltirone increased caspase-3/8 activity as well as B-cell lymphoma 2-associated X-protein, apoptosis-inducing factor (AIF), p53 and poly(ADP-ribose) polymerase (PARP) protein expression, whereas it inhibited mitochondrial reactive oxygen species (ROS) generation and matrix metalloproteinase (MMP)-2/9 protein expression in HCC827 and A549 platinum-resistant lung cancer cells. The results of the present study demonstrated that miltirone induces apoptosis in cisplatin-resistant lung cancer cells through ROS-p53, AIF, PARP and MMP2/9 signaling pathways.

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Knockdown of hepatoma-derived growth factor-related protein-3 induces apoptosis of H1299 cells via ROS-dependent and p53-independent NF-κB activation

Cited by 12 publications

References 17 publications

Artocarpin, an isoprenyl flavonoid, induces p53-dependent or independent apoptosis via ROS-mediated MAPKs and Akt activation in non-small cell lung cancer cells

Artocarpin, an isoprenyl flavonoid, induces p53-dependent or independent apoptosis via ROS-mediated MAPKs and Akt activation in non-small cell lung cancer cells

Evidence of altered depression and dementia‐related proteins in the brains of young rats after ovariectomy

Miltirone‑induced apoptosis in cisplatin‑resistant lung cancer cells through upregulation of p53 signaling pathways

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