Cold atmospheric plasma and iron oxide-based magnetic nanoparticles for synergetic lung cancer therapy

Li, Wentong; Yu, Hongli; Ding, Dejun; Chen, Zhitong; Wang, Yonghong; Wang, Saisai; Li, Xujing; Keidar, Michael; Zhang, Weifen

doi:10.1016/j.freeradbiomed.2018.10.429

Cited by 98 publications

(76 citation statements)

References 54 publications

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“…Clinical data from several available cohorts, including TCGA and meta-base 1000 patients with lung cancer, indicated that the ALDOA-Oct4-TRAF4/DUSP4 axis is a potential prognostic indicator and may be a therapeutic target. In non-small cell lung cancer, scientists are developing various strategies and methods for targeting and specificity 42,43 . This finding has strong potential for the development of novel cancer therapies or combination therapies against CSCs in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Nonenzymatic function of Aldolase A downregulates miR-145 to promote the Oct4/DUSP4/TRAF4 axis and the acquisition of lung cancer stemness

et al. 2020

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Drug resistance remains a serious issue of clinical importance and is a consequence of cancer stemness. In this study, we showed that the level of Aldolase A (ALDOA) expression is significantly associated with the IC50 value of chemotherapy drugs in lung cancer. Our data revealed that ALDOA overexpression resulted in a significant increase of lung tumor spheres. The use of ingenuity pathway analysis (IPA) resulted in the identification of POU5F1 (Oct4) as the leading transcription factor of ALDOA. We observed high expression of ALDOA, Oct4 and stemness markers in collected spheroid cells. DUSP4 and TRAF4 were confirmed as major downstream targets of the ALDOA-Oct4 axis. Knockdown of these molecules significantly decreased the stemness ability of cells. In addition, we investigated whether miR-145 targets the 3′-UTR of Oct4 and is regulated by ALDOA due to the involvement of ALDOA in glycolysis and metabolic reprogramming. Furthermore, we constructed several mutant forms of ALDOA that disrupted its enzymatic activity and showed that they still induced significant in vitro sphere formation and in vivo tumorigenicity. These results demonstrated that ALDOA-mediated spheroid formation is independent of its enzymatic activity. In the clinical component, we also showed that the combination of ALDOA and TRAF4 or DUSP4 is positively correlated with poor overall survival in a xenograft model and cancer patients through immunohistochemical analyses. The results of our study revealed novel functional roles of ALDOA in inducing cancer stemness via the inhibition of miR-145 expression and the activation of Oct4 transcription. These findings offer new therapeutic strategies for modulation of lung cancer stemness to enhance chemotherapeutic responses in lung cancer patients.

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Section: Discussionmentioning

confidence: 99%

Nonenzymatic function of Aldolase A downregulates miR-145 to promote the Oct4/DUSP4/TRAF4 axis and the acquisition of lung cancer stemness

et al. 2020

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“…Currently, there are many studies focusing on the proliferation and apoptosis of NSCLC cells, aiming to obtain more effective treatments 32 . Randomized trials show that PEM has a good therapeutic effect and has become a preferential drug for patients with NSCLC 33,34 .…”

Section: Discussionmentioning

confidence: 99%

YIPF2 promotes chemotherapeutic agent-mediated apoptosis via enhancing TNFRSF10B recycling to plasma membrane in non-small cell lung cancer cells

Wang

Guo

et al. 2020

Cell Death Dis

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Non-small cell lung cancer (NSCLC) is the most common histological type of lung cancer, and the identification of the apoptotic process of NSCLC is vital for its treatment. Usually, both the expression level and the cell surface level of TNFRSF10B (TNF Receptor superfamily member 10B) will increase after treatment with some chemotherapeutic agents, which plays a critical role in the apoptosis induction. However, the exact molecular mechanism underlying TNFRSF10B regulation remains largely elusive. Here, we found that TNFRSF10B, along with a vesicular trafficking regulator protein, YIPF2, were upregulated after treatment with pemetrexed (PEM) in NSCLC cells. Besides, YIPF2 increased the surface level of TNFRF10B, while YIPF2 knockdown inhibited the upregulation of TNFRSF10B and its recycling to plasma membrane. In addition, RAB8 decreased the cell surface TNFRSF10B by promoting its removing from plasma membrane to cytoplasm. Furthermore, we found that YIPF2, RAB8 and TNFRSF10B proteins interacted physically with each other. YIPF2 could further inhibit the physical interaction between TNFRSF10B and RAB8, thereby suppressing the removing of TNFRSF10B from plasma membrane to cytoplasm mediated by RAB8 and maintaining its high level on cell surface. Finally, using bioinformatics database, the YIPF2-TNFRSF10B axis was confirmed to be associated with the malignant progression of lung cancer. Taken together, we show that YIPF2 promotes chemotherapeutic agentmediated apoptosis via enhancing TNFRSF10B recycling to plasma membrane in NSCLC cells. These findings may be beneficial for the development of potential prognostic markers of NSCLC and may provide effective treatment strategy.

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“…CAP was initially used for decontamination [ 3 ] and wound healing, [ 4 ] and its anticancer potential was revealed in the last decade. Ever since the early reports on the oncotherapeutic potential of CAP were delineated, its selectivity against cancer cells has been discovered for various cancers, including melanoma, [ 2 ] colon cancer, [ 5,6 ] lung cancer, [ 7 ] hepatocellular carcinoma, [ 8 ] breast cancer, [ 9 ] ovarian cancer, [ 10 ] cervical cancer, [ 11 ] glioblastoma, [ 12 ] pancreatic cancer, [ 13,14 ] head and neck cancer, [ 15 ] and leukemia [ 14 ] (Table 1). Previous studies revealed the variation of the plasma selectivity for different breast cancer subtypes subjected to appropriate dosing control.…”

Section: Introductionmentioning

confidence: 99%

Dosing: The key to precision plasma oncology

Dai

Zhang

et al. 2020

Plasma Processes & Polymers

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Cold atmospheric plasma (CAP) is an emerging oncotherapeutic approach with selectivity for cancer cells. It can induce different cell survival and death programs depending on the CAP dose, and it can function as a neo or adjuvant therapy against cancer. Establishing an evaluation system for precise CAP dosing is the key to make plasma therapy act alone or in combination with other therapeutic modalities for achieving desirable treatment responses. By classifying CAP-induced effects and associating them with the dosing of plasma-reactive agents, we identify opportunities for CAP to contribute to precision oncotherapy and discuss challenges en route to clinical applications. We emphasize the importance of dosing in plasma medicine and encourage crossdisciplinary collaborations to develop suitable dosing metrics.

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Cold atmospheric plasma and iron oxide-based magnetic nanoparticles for synergetic lung cancer therapy

Cited by 98 publications

References 54 publications

Nonenzymatic function of Aldolase A downregulates miR-145 to promote the Oct4/DUSP4/TRAF4 axis and the acquisition of lung cancer stemness

Nonenzymatic function of Aldolase A downregulates miR-145 to promote the Oct4/DUSP4/TRAF4 axis and the acquisition of lung cancer stemness

YIPF2 promotes chemotherapeutic agent-mediated apoptosis via enhancing TNFRSF10B recycling to plasma membrane in non-small cell lung cancer cells

Dosing: The key to precision plasma oncology

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