|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | The role of exosomal long non-coding RNAs in cancer drug resistance显示文摘One of the major challenges in oncology is drug resistance,which triggers relapse and shortens patients’survival.In order to promote drug desensitization,cancer cells require the establishment of an ideal tumor microenvironment that accomplishes specific conditions.To achieve this objective,cellular communication is a key factor.Classically,cells were believed to restrictively communicate by ligand-receptor binding,physical cell-to-cell interactions and synapses.Nevertheless,the crosstalk between tumor cells and stroma cells has also been recently reported to be mediated through exosomes,the smallest extracellular vesicles,which transport a plethora of functionally active molecules,such as:proteins,lipids,messenger RNA,DNA,microRNA or long non-coding RNA(lncRNAs).LncRNAs are RNA molecules greater than 200 base pairs that are deregulated in cancer and other diseases.Exosomal lncRNAs are highly stable and can be found in several body fluids,being considered potential biomarkers for tumor liquid biopsy.Exosomal lncRNAs promote angiogenesis,cell proliferation and drug resistance.The role of exosomal lncRNAs in drug resistance affects the main treatment strategies in oncology:chemotherapy,targeted therapy,hormone therapy and immunotherapy.Overall,knowing the molecular mechanisms by which exosomal lncRNA induce pharmacologic resistance could improve further drug development and identify drug resistance biomarkers. | Mireia Cruz De los Santos Mihnea P.Dragomir George A.Calin | 2019 | Cancer Drug Resistance2019，2，4： | 3 |
| 2 | Targeting non-coding RNAs to overcome cancer therapy resistance显示文摘It is now well known that non-coding RNAs(ncRNAs),rather than protein-coding transcripts,are the preponderant RNA transcripts.NcRNAs,particularly microRNAs(miRNAs),long non-coding RNAs(lncRNAs),and circular RNAs(circRNAs),are widely appreciated as pervasive regulators of multiple cancer hallmarks such as proliferation,apoptosis,invasion,metastasis,and genomic instability.Despite recent discoveries in cancer therapy,resistance to chemotherapy,radiotherapy,targeted therapy. | BaoQing Chen Mihnea P.Dragomir Chen Yang Qiaoqiao Li David Horst George A.Calin | 2022 | Signal Transduction and Targeted Therapy2022，7，5： | 3 |
| 3 | Key questions about the checkpoint blockade-are microRNAs an answer?显示文摘The introduction of immune-checkpoint blockade in the cancer therapy led to a paradigm change of the management of late stage cancers. There are already multiple FDA approved checkpoint inhibitors and many other agents are undergoing phase 2 and early phase 3 clinical trials. The therapeutic indication of immune checkpoint inhibitors expanded in the last years, but still remains unclear who can benefit. Micro RNAs are small RNAs with no coding potential. By complementary pairing to the 3' untranslated region of messenger RNA, microRNAs exert posttranscriptional control of protein expression. A network of microRNAs directly and indirectly controls the expression of checkpoint receptors and several microRNAs can target multiple checkpoint molecules,mimicking the therapeutic effect of a combined immune checkpoint blockade. In this review, we will describe the microRNAs that control the expression of immune checkpoints and we will present four specific issues of the immune checkpoint therapy in cancer:(1) imprecise therapeutic indication,(2) difficult response evaluation,(3) numerous immunologic adverse-events, and(4)the absence of response to immune therapy. Finally, we propose microRNAs as possible solutions for these pitfalls. We consider that in the near future microRNAs could become important therapeutic partners of the immune checkpoint therapy. | Mihnea Dragomir Baoqing Chen Xiao Fu George A.Calin | 2018 | Cancer Biology & Medicine2018，15，2： | 2 |
| 4 | Gut microbiota:a new player in regulating immune-and chemo-therapy efficacy显示文摘Development of drug resistance represents the major cause of cancer therapy failure,determines disease progression and results in poor prognosis for cancer patients.Different mechanisms are responsible for drug resistance.Intrinsic genetic modifications of cancer cells induce the alteration of expression of gene controlling specific pathways that regulate drug resistance:drug transport and metabolism;alteration of drug targets;DNA damage repair;and deregulation of apoptosis,autophagy,and pro-survival signaling.On the other hand,a complex signaling network among the entire cell component characterizes tumor microenvironment and regulates the pathways involved in the development of drug resistance.Gut microbiota represents a new player in the regulation of a patient’s response to cancer therapies,including chemotherapy and immunotherapy.In particular,commensal bacteria can regulate the efficacy of immune checkpoint inhibitor therapy by modulating the activation of immune responses to cancer.Commensal bacteria can also regulate the efficacy of chemotherapeutic drugs,such as oxaliplatin,gemcitabine,and cyclophosphamide.Recently,it has been shown that such bacteria can produce extracellular vesicles(EVs)that can mediate intercellular communication with human host cells.Indeed,bacterial EVs carry RNA molecules with gene expression regulatory ability that can be delivered to recipient cells of the host and potentially regulate the expression of genes involved in controlling the resistance to cancer therapy.On the other hand,host cells can also deliver human EVs to commensal bacteria and similarly,regulate gene expression.EVmediated intercellular communication between commensal bacteria and host cells may thus represent a novel research area into potential mechanisms regulating the efficacy of cancer therapy. | Simone Anfossi George A.Calin | 2020 | Cancer Drug Resistance2020，3，3： | 1 |
| 5 | Plasma microRNA 210 levels correlate with sensitivity to trastuzumab and tumor presence in breast cancer patients显示文摘 | Eun‐JungJung LiberoSantarpia JuyeonKim Francisco J.Esteva EricaMoretti Aman U.Buzdar AngeloDi Leo Xiao‐FengLe Robert C.Bast Soon‐TaePark LajosPusztai George A.Calin | 2012 | Cancer2012，，10： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员