Hepatitis B virus (HBV) infection is regarded as the main etiological risk factor in the process of hepatocellular carcinoma (HCC), as it promotes an immunosuppressive microenvironment that is partially mediated by the programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling pathway. The tumor microenvironment (TME) of HBV-related HCC is indeed more immunosuppressive than microenvironments not associated with viruses. And compared to TME in hepatitis C virus (HCV) infected HCC, TME of HBV-related HCC is less vascularized and presents different immune components resulting in similar immunosuppression. However, few studies are focusing on the specific side effects and efficacy of PD-1/PD-L1 blockade immunotherapy in HBV-related HCC patients, as well as on the underlying mechanism. Herein, we reviewed the basic research focusing on potential TME alteration caused by HBV infection, especially in HCC patients. Moreover, we reviewed PD-1/PD-L1 blockade immunotherapy clinical trials to clarify the safety and efficacy of this newly developed treatment in the particular circumstances of HBV infection. We found that patients with HBV-related HCC displayed an acceptable safety profile similar to those of non-infected HCC patients. However, we could not determine the antiviral activity of PD-1/PD-L1 blockade because standard anti-viral therapies were conducted in all of the current clinical trials, which made it difficult to distinguish the potential influence of PD-1/PD-L1 blockade on HBV infection. Generally, the objective response rates (ORRs) of PD-1/PD-L1 blockade immunotherapy did not differ significantly between virus-positive and virus-negative patients, except that disease control rates (DCRs) were obviously lower in HBV-infected HCC patients.
Cancer stem cells (CSCs) play a vital role in the formation of tumors and have been studied as a target of anticancer therapy. Long non-coding RNAs (lncRNAs) are important in the genesis and progression of cancer. Various lncRNAs, such as ROR, HOTAIR, H19, UCA1, and ARSR, are involved in cancer stemness. These lncRNAs could regulate the expression of CSC-related transcriptional factors, such as SOX2, OCT4, and NANOG, in colorectal, prostate, bladder, breast, liver, and other cancer types. In this work, we review the progress of lncRNAs and cancer stem cells and discuss the potential signal pathways of lncRNAs in cancer stemness.
Radiotherapy is one of the main modalities of cancer treatment. However, tumor recurrence following radiotherapy occurs in many cancer patients. A key to solving this problem is the optimization of radiosensitivity. In recent years, long non-coding RNAs (lncRNAs), which affect the occurrence and development of tumors through a variety of mechanisms, have become a popular research topic. LncRNAs have been found to influence radiosensitivity by regulating various mechanisms, including DNA damage repair, cell cycle arrest, apoptosis, cancer stem cells regulation, epithelial–mesenchymal transition, and autophagy. LncRNAs are expected to become a potential therapeutic target for radiotherapy in the future. This article reviews recent advances in the role and mechanism of lncRNAs in tumor radiosensitivity.
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