Insufficient radiofrequency ablation promotes the growth of non-small cell lung cancer cells through PI3K/Akt/HIF-1&amp;alpha; signals

Wan, Jun; Wu, Wei; Chen, Yun; Kang, Ningning; Zhang, Renquan

doi:10.1093/abbs/gmw005

Cited by 22 publications

(14 citation statements)

References 26 publications

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“…31 IL-2 treatment in the form of a fusion protein bound to a tumourspecific antibody was shown to enhance antitumour immunity against colon tumours treated with RFA. 32 Insufficient RFA has also been shown to promote angiogenesis of residual HCC 33 and promote tumour growth of non-small cell lung cancer cells 34 via HIF-1a/VEGFA. Subtotal ablation can also induce hepatic regeneration and tumorigenesis via IL-6, c-met, or HGF-dependent pathways.…”

Section: B Amentioning

confidence: 99%

Combined locoregional-immunotherapy for liver cancer

Greten

Mauda-Havakuk

Heinrich

et al. 2019

Journal of Hepatology

153

111

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Locoregional therapies are commonly used to treat patients with hepatocellular carcinoma. It has been noted for many years that locoregional therapies may have additional systemic effects other than simple tumour elimination. Immunological ''side effects" have been described in response to locoregional therapies in animal studies and in patients. With the advent of immunotherapy for hepatocellular carcinoma, there is increasing interest in determining the best way to combine immunotherapy with locoregional therapies. Herein, we provide a compact summary of answered and unanswered questions in the field, including: What animal model is best suited to test combined immune-locoregional treatments? How does tumour cell death affect immune responses? What type of immune responses have been observed in patients treated with different types of locoregional therapies? What can be surmised from the results of the first study testing the combination of locoregional therapy with immune checkpoint blockade? Finally, we discuss the outlook for this rapidly growing area of research, focussing on the issues which must be overcome to bridge the gap between interventional radiology and cancer immunology. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver.

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Section: B Amentioning

confidence: 99%

Combined locoregional-immunotherapy for liver cancer

Greten

Mauda-Havakuk

Heinrich

et al. 2019

Journal of Hepatology

153

111

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“…In hypoxic tumor cells, HIF-1α expression can be facilitated by PI3K/AKT signaling. Abnormal PI3K/AKT signaling may result in increased or uncontrolled cell proliferation in tumors [17]. …”

Section: Introductionmentioning

confidence: 99%

Celecoxib Down-Regulates the Hypoxia-Induced Expression of HIF-1α and VEGF Through the PI3K/AKT Pathway in Retinal Pigment Epithelial Cells

Sun¹,

Cai²,

Liu³

2017

Cell Physiol Biochem

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Background/Aims: The goal of this study was to detect the expression of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in human retinal pigmented epithelial (RPE) cells treated with celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, under hypoxic and normoxic conditions and to explore the signaling mechanism involved in regulating the hypoxia-induced expression of HIF-1α and VEGF in RPE cells. Methods: D407 cells were cultured in normoxic or hypoxic conditions, with or without celecoxib or a PI3K inhibitor (LY294002). The anti-proliferative effect of celecoxib was assessed using the MTT assay. RT-PCR, Western blotting and ELISA were performed to detect the levels of PI3K, phosphorylated AKT (p-AKT), HIF-1α, VEGF and COX-2. Results: Celecoxib inhibited the proliferation of RPE cells in a dose-dependent manner. Celecoxib suppressed the expression of VEGF at both the mRNA and protein levels and decreased HIF-1α protein expression. HIF-1α activation was regulated by the PI3K/AKT pathway. The celecoxib-induced down-regulation of HIF-1α and VEGF required the suppression of the hypoxia-induced PI3K/AKT pathway. However, the down-regulation of COX-2 did not occur in cells treated with celecoxib. Conclusions: The antiangiogenic effects of celecoxib in RPE cells under hypoxic conditions resulted from the inhibition of HIF-1α and VEGF expression, which may be partly mediated by a COX-2-independent, PI3K/AKT-dependent pathway.

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“…In another report, microRNA-223 was identified as a potential therapeutic target for overcoming epidermal growth factor receptor-tyrosine kinase inhibitor resistance, owing to its function in inducing activation of the PI3K/AKT/mTOR signaling pathway in PC9/ER and PC9/CD133+ cells, which is responsible for the resistance of PC9/ER and PC9/CD133+ cells to erlotinib (26). Additionally, a study by Wan et al suggested that insufficient RFA activates tumor growth in vitro and in vivo via PI3K/AKT/mTOR signals (27).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of TM7SF4 inhibits cell proliferation and metastasis of A549 cells through regulating the PI3K/AKT/mTOR signaling pathway

Yang

Song

Wang

et al. 2017

Molecular Medicine Reports

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Lung cancer is one of the most common types of malignant tumor worldwide. The etiology of lung cancer is complex and, although significant progress has been made in previous investigations, the molecular mechanism responsible for lung cancer remains to be fully elucidated. In the present study, the association between lung cancer and transmembrane 7 superfamily member 4 (TM7SF4) was investigated. Reverse transcription‑quantitative polymerase chain reaction technology was used to detect the expression of TM7SF4, and it was expressed at a high level in lung cancer. Furthermore, by overexpressing and inhibiting the expression of TM7SF4, the present study compared cell proliferation and migration rates. It was confirmed that TM7SF4 promoted lung cancer cell proliferation and migration. TM7SF4 was also confirmed to promote cancer cell migration and invasion by modulating the activation of the phosphatidylinositol 3‑kinase/Akt pathway in the A549 cells. Correspondingly, the inhibition of TM7SF4 decreased the expression of proteins associated with AKT, whereas the overexpression of TM7SF4 promoted the expression of the relevant proteins. Therefore, the present study confirmed that TM7SF4 was involved in the progression of lung cancer via regulating the activation of AKT. These findings suggested that TM7SF4 may be involved in the progression of lung cancer and may be a novel therapeutic target for this disease.

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Insufficient radiofrequency ablation promotes the growth of non-small cell lung cancer cells through PI3K/Akt/HIF-1α signals

Cited by 22 publications

References 26 publications

Combined locoregional-immunotherapy for liver cancer

Combined locoregional-immunotherapy for liver cancer

Celecoxib Down-Regulates the Hypoxia-Induced Expression of HIF-1α and VEGF Through the PI3K/AKT Pathway in Retinal Pigment Epithelial Cells

Downregulation of TM7SF4 inhibits cell proliferation and metastasis of A549 cells through regulating the PI3K/AKT/mTOR signaling pathway

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