MicroRNA-26a suppresses epithelial-mesenchymal transition in human hepatocellular carcinoma by repressing enhancer of zeste homolog 2

Ma, Dongjie; Chai, Zong‐Tao; Zhu, Xiao‐Dong; Zhang, Ning; Zhan, Di-Hua; Ye, Bo‐Gen; Wang, Cheng-Hao; Qin, Chengdong; Zhao, Yiming; Zhu, Weiping; Cao, Manqing; Gao, Dongmei; Sun, Hui‐Chuan; Tang, Zhao–You

doi:10.1186/s13045-015-0229-y

Cited by 139 publications

(105 citation statements)

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“…Repeated biopsy showed that it may be responsible for half of acquired resistance cases 65. Several third‐generation EGFR TKIs have been developed particularly target the T790M mutation, including HM61713, EGF816, and ASP8273, with response rates ranging from 31% to 54% 66. The objective response rate (ORR) of osimertinib is over 60%, which has been confirmed in a phase I study and two phase II studies.…”

Section: The Mechanism Of Brain Metastasismentioning

confidence: 90%

Emerging findings into molecular mechanism of brain metastasis

Chen

2018

Cancer Medicine

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Brain metastasis is an important cause of morbidity and mortality in cancer patients. Hence, the need to develop improved therapies to prevent and treat metastasis to the brain is becoming urgent. Recent studies in this area are bringing about some advanced progress on brain metastasis. It was concluded that the occurrence and poor prognosis of brain metastasis have been mostly attributed to the exclusion of anticancer drugs from the brain by the blood‐brain barrier. And several highly potent new generation targeted drugs with enhanced CNS distribution have been developed constantly. However, the noted “seed and soil” hypothesis also suggests that the outcome of metastasis depends on the relationship between unique tumor cells and the specific organ microenvironment. Moreover, increasing studies in multiple tumor types demonstrated that brain metastasis has great molecular differences between primary tumors and extracranial metastasis to a large extent. Here, the authors summarized the most common malignancies that could lead to brain metastasis—lung cancer, breast cancer and melanoma and their related mutated factors. Only by comprehending a deeper understanding of the molecular mechanisms, more effective brain‐specific therapies will be developed for brain metastasis.

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Section: The Mechanism Of Brain Metastasismentioning

confidence: 90%

Emerging findings into molecular mechanism of brain metastasis

Chen

2018

Cancer Medicine

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“…Prior patient consent from each participant and ethical approval from the Research Ethics Committee of Fudan University Shanghai Cancer Center were obtained. The detailed follow-up procedures were described previously [28, 29]. …”

Section: Methodsmentioning

confidence: 99%

Monoacylglycerol lipase promotes progression of hepatocellular carcinoma via NF-κB-mediated epithelial-mesenchymal transition

et al. 2016

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BackgroundMonoacylglycerol lipase (MAGL), a critical lipolytic enzyme, has emerged as a key regulator of tumor progression, yet its biological function and clinical significance in hepatocellular carcinoma (HCC) is still unknown.MethodsIn this study, we used a tissue microarray containing samples from 170 HCC patients to evaluate the expression of MAGL and its correlation with other clinicopathologic characteristics. In addition, we investigated the regulating effects of MAGL on various HCC lines. Finally, we identified the NF-κB signaling pathway participated in MAGL-mediated epithelial-mesenchymal transition (EMT) using HCC cell lines with different metastatic potentials.ResultsThe expression of MAGL was significantly higher in HCC tumors than in matched peritumor tissues. Specifically, high MAGL expression was found in tumors with larger tumor size, microvascular invasion, poor differentiation, or advanced TNM stage. In addition, the clinical prognosis for the MAGLhigh group was markedly poorer than that for the MAGLlow group in the 1-, 3-, and 5-year overall survival times and recurrence rates of HCC patients. MAGL expression was an independent prognostic factor for both survival and recurrence after curative resection. Furthermore, the upregulation of MAGL in HCC cells promoted cell growth and invasiveness abilities, and accompanied by EMT. In contrast, downregulation of MAGL obviously inhibited these characteristics. Moreover, further investigations verified that MAGL facilitates HCC progression via NF-κB-mediated EMT process.ConclusionsOur findings demonstrate MAGL could promote HCC progression by the induction of EMT and suggest a potential therapeutic target, as well as a biomarker for prognosis, in patients with HCC.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-016-0361-3) contains supplementary material, which is available to authorized users.

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“…Already, the field has witnessed significant toxicities from CD19-CAR-T therapies that efficiently clear B-cell malignancies, but trigger severe (though reversible) cytokine release syndrome [14] and neurotoxicities, along with deletion of normal B-cells [76]. The current generation of CD19-CAR-T therapies lack built-in safety mechanisms.…”

Section: Engineering Safety and Specificity Into T-cell Therapymentioning

confidence: 99%

Strategies for enhancing adoptive T-cell immunotherapy against solid tumors using engineered cytokine signaling and other modalities

Shum

Kruse²,

Rooney³

2018

Expert Opinion on Biological Therapy

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Introduction: Cancer therapy has been transformed by the demonstration that tumor-specific T-cells can eliminate tumor cells in a clinical setting with minimal long-term toxicity. However significant success in the treatment of leukemia and lymphoma with T-cells using native receptors or redirected with chimeric antigen receptors (CARs) has not been recapitulated in the treatment of solid tumors. This lack of success is likely related to the paucity of costimulatory and cytokine signaling available in solid tumors, in addition to a range of inhibitory mechanisms. Areas covered: We summarize the latest developments in engineered T-cell immunotherapy, describe the limitations of these approaches in treating solid tumors, and finally highlight several strategies that may be useful in mediating solid tumor responses in the future, while also ensuring safety of engineered cells. Expert opinion: CAR-T therapies require further engineering to achieve their potential against solid tumors. Facilitating cytokine signaling in CAR T-cells appears to be essential in achieving better responses. However, the engineering of T-cells with potentially unchecked proliferation and potency raises the question of whether the simultaneous combination of enhancements will prove safe, necessitating continued advancements in regulating CAR-T activity at the tumor site and methods to safely switch off these engineered cells.

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MicroRNA-26a suppresses epithelial-mesenchymal transition in human hepatocellular carcinoma by repressing enhancer of zeste homolog 2

Cited by 139 publications

References 50 publications

Emerging findings into molecular mechanism of brain metastasis

Emerging findings into molecular mechanism of brain metastasis

Monoacylglycerol lipase promotes progression of hepatocellular carcinoma via NF-κB-mediated epithelial-mesenchymal transition

Strategies for enhancing adoptive T-cell immunotherapy against solid tumors using engineered cytokine signaling and other modalities

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