Publications by authors named "Mubalake Abudoureyimu"

Unlabelled: Hepatocellular carcinoma (HCC) is a highly malignant tumor with a global prevalence. In addition to the existing clinical guidelines, the effectiveness of anlotinib and Aurora-A inhibitors in treating HCC has also been demonstrated. However, Anlotinib, as an anti-angiogenesis therapy, has shown significant benefits in clinical trials but is limited by its single-agent treatment and the development of drug resistance.

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Linc-ROR have been well-demonstrated to play important roles in cancer progression and angiogenesis. However, the underlying oncogenic mechanism of Linc-ROR in hepatocellular carcinoma is poorly understood. In this study, we demonstrate that Linc-ROR plays an oncogenic role in part through its positive regulation of DEPDC1 expression.

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Reprogramming of metabolism is one of the hallmarks of cancer, among which glucose metabolism dysfunction is the most prominent feature. The glucose metabolism of tumor cells is significantly different from that of normal cells. Glucose metabolism reprogramming of hepatocellular carcinoma (HCC) has become an important research hotspot in the field of HCC, a variety of tumor metabolic interventions have been applied clinically.

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Aurora-A is a mitotic serine/threonine-protein kinase and an oncogene. In normal cells, Aurora-A appears from G2 phase and localizes at the centrosome, where it participates in centrosome replication, isolation and maturation. Aurora-A also maintains Golgi apparatus structure and spindle assembly.

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Background: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed solid cancer and the main origin of cancer-related deaths worldwide. Current strategies to treat advanced NSCLC are based on a combined approach of targeted therapy and chemotherapy. But most patients will eventually get resistance to either chemotherapy or targeted therapy, leading to the poor prognosis.

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Hepatocellular carcinoma (HCC) is one of the most frequent cancers worldwide, particularly in China. Despite the development of HCC treatment strategies, the survival rate remains unpleasant. Gene-targeted oncolytic viral therapy (GTOVT) is an emerging treatment modality-a kind of cancer-targeted therapy-which creates viral vectors armed with anti-cancer genes.

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As the first oral multi-target anti-tumor drug proved for the treatment of patients with advanced liver cancer in 2007, sorafenib has changed the landscape of advanced hepatocellular carcinoma (HCC) treatment. However, drug resistance largely hinders its clinical application. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), and long non-coding (lncRNAs), have recently been demonstrated playing critical roles in a variety of cancers including HCC, while the mechanisms of ncRNAs in HCC sorafenib resistance have not been extensively characterized yet.

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-associated death worldwide. Indeed, despite the benefit of sorafenib in the treatment of some patients with HCC, the majority of these patients have a poor response to or intolerance of sorafenib, resulting in further tumor progression. Exploring the mechanisms underlying sorafenib resistance is essential to the treatment of HCC.

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Exosomes are small membrane vesicles 50-150 nm in diameter released by a variety of cells, which contain miRNAs, mRNAs and proteins with the potential to regulate signalling pathways in recipient cells. Exosomes deliver nucleic acids and proteins to participate in orchestrating cell-cell communication and microenvironment modulation. In this review, we summarize recent progress in our understanding of the role of exosomes in hepatocellular carcinoma (HCC).

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MicroRNAs are small non-coding RNAs that play critical roles in the regulatory mechanisms involving cell differentiation, proliferation, apoptosis and tumorigenesis. Recent research efforts have been conducted to apply these discoveries into clinical functions, including the early diagnosis and therapeutic outcome of patients with cancer. Previous studies have shown that microRNA-149 (miR-149) is dysregulated in various human cancers and exerts its effects on tumorigenesis and tumour progression.

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