Loss of AR-regulated AFF3 contributes to prostate cancer progression and reduces ferroptosis sensitivity by downregulating ACSL4 based on single-cell sequencing analysis.

Prostate cancer (PCa) is one of the most common cancers affecting the health of men worldwide. Castration-resistant prostate cancer (CRPC), the advanced and refractory phase of prostate cancer, has multiple mechanisms of resistance to androgen deprivation therapy (ADT) such as AR mutations, aberrant androgen synthase, and abnormal expression of AR-related genes. Based on the research of the AR pathway, new drugs for the treatment of CRPC have been developed in clinical practice, such as Abiraterone and enzalutamide. However, many areas in this pathway are still worth exploring. In this study, single-cell sequencing analysis was utilized to scrutinize significant genes in the androgen receptor (AR) pathway related to CRPC. Our analysis of single-cell sequencing combined with bulk-cell sequencing revealed a substantial downregulation of AR-regulated AFF3 in CRPC. Overexpression of AFF3 restricted the proliferation and migration of prostate cancer cells whilst also increasing their sensitivity towards enzalutamide, while knockdown of AFF3 had the opposite effect. To elucidate the mechanism of tumor inhibition by AFF3, we applied GSVA and GSEA to investigate the metabolic pathways related to AFF3 and revealed that AFF3 had an impact on fatty acids metabolism and ferroptosis through the regulation of ACSL4 protein expression. Based on correlation analysis and flow cytometry, we can speculate that AFF3 can impact the sensitivity of the CRPC cell lines to the ferroptosis inducer (RSL3) by regulating ACSL4. Therefore, our findings may provide new insights into the mechanisms of drug resistance in CRPC, and AFF3 may serve as a novel prognostic biomarker in prostate cancer.

Electrochemical Synthesis of the Energetic Combustion Catalyst Co(BODN)·9H2O and Its Catalytic Effect on Ammonium Perchlorate Thermal Decomposition.

Safe, efficient, and green synthetic energetic combustion catalysts are of great importance for the application of ammonium perchlorate (AP) in solid propellants. In this study, a novel, simple, efficient, and green electrochemical method for synthesizing energetic combustion catalysts was designed and implemented to successfully synthesize Co(BODN)·9H2O (BODN = [2,2'-bi{1,3,4-oxadiazole}]-5,5'-dinitramide), a novel energetic combustion catalyst. The target products were characterized via single-crystal X-ray diffraction, powder X-ray diffraction, Fourier transform infrared spectroscopy, optical microscopy, scanning electron microscopy, differential scanning calorimetry, and thermogravimetric analysis. Results reveal that Co(BODN)·9H2O crystallizes in the triclinic P1̅ space group and has a density of 1.836 g cm-3. The size of the Co(BODN)·9H2O crystal increases gradually with the increase in the reaction current and the prolongation of the reaction time, respectively. However, the change in reaction current and time does not affect the crystal form. In addition, with the increase in Co(BODN)·9H2O content, the peak temperature of high-temperature decomposition (HTD) and apparent activation energy of AP/Co(BODN)·9H2O gradually decrease, and the heat release during thermal decomposition gradually increases. The HTD peak temperature and apparent activation energy of AP/Co(BODN) 9H2O (10%) decrease by 97.9 °C and 94.2 kJ·mol-1, respectively, compared with those of pure AP, and the heat release during thermal decomposition increases by 1613 J·g-1. Furthermore, compared with those of the propellant containing pure AP, the burning rate and flame temperature of the propellant containing AP/Co(BODN)·9H2O (10%) increase by 8.15 mm s-1 and 458.44 °C, respectively. Real-time Fourier transform infrared spectroscopy reveals that CoO catalyzes the thermal decomposition of AP mainly by promoting electron transfer to accelerate the oxidation of NH3 and the conversion of N2O to NO. In brief, this work provides new insights into synthesizing energetic combustion catalysts. Moreover, Co(BODN)·9H2O synthesized through the electrochemical method exhibits considerable application prospects for improving the thermal and energy performance of AP and the combustion performance of propellants.

The role of DDX46 in breast cancer proliferation and invasiveness: A potential therapeutic target.

DDX46, a member of DEAD-box (DDX) proteins, is associated with various cancers, while its involvement in the pathogenesis of breast cancer hasn't been reported so far. The study demonstrated the overexpression of DDX46 in human breast cancer cells and tissue samples, and correlated with high histological grade and lymph node metastasis. Downregulation of DDX46 in the breast cancer cell lines inhibited their proliferation and invasiveness in vitro. Furthermore, the growth of MDA-MB-231 xenografts was suppressed in nude mice by DDX46 knockingdown. Taken together, our findings suggest that DDX46 is an oncogenic factor in human breast cancer, and a potential therapeutic target.

The role of noncoding RNAs in the tumor microenvironment of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the leading fatal malignancy worldwide. The tumor microenvironment (TME) can affect the survival, proliferation, migration, and even dormancy of cancer cells. Hypoxia is an important component of the TME, and hypoxia-inducible factor-1α (HIF-1α) is the most important transcriptional regulator. Noncoding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), comprise a large part of the human transcriptome and play an important role in regulating the tumorigenesis of HCC. This review discusses the role of ncRNAs in hepatocarcinogenesis, epithelial-mesenchymal transition (EMT), and angiogenesis in a hypoxic microenvironment, as well as the interactions between ncRNAs and key components of the TME. It further discusses their use as biomarkers and the potential clinical value of drugs, as well as the challenges faced in the future.

Functions of non-coding RNAs in regulating cancer drug targets.

With the development of precision medicine, the efficiency of tumor treatment has been significantly improved. More attention has been paid to targeted therapy and immunotherapy as the key to precision treatment of cancer. Targeting epidermal growth factor receptor (EGFR) has become one of the most important targeted treatments for various cancers. Comparing with traditional chemotherapy drugs, targeting EGFR is highly selective in killing tumor cells with better safety, tolerability and less side effect. In addition, tumor immunotherapy has become the fourth largest tumor therapy after surgery, radiotherapy and chemotherapy, especially immune checkpoint inhibitors. However, these treatments still produce a certain degree of drug resistance. Non-coding RNAs (ncRNAs) were found to play a key role in carcinogenesis, treatment and regulation of the efficacy of anticancer drugs in the past few years. Therefore, in this review, we aim to summarize the targeted treatment of cancers and the functions of ncRNAs in cancer treatment.

miR-199a: A Tumor Suppressor with Noncoding RNA Network and Therapeutic Candidate in Lung Cancer.

Lung cancer is the leading cause of cancer death worldwide. miR-199a, which has two mature molecules: miR-199a-3p and miR-199a-5p, plays an important biological role in the genesis and development of tumors. We collected recent research results on lung cancer and miR-199a from Google Scholar and PubMed databases. The biological functions of miR-199a in lung cancer are reviewed in detail, and its potential roles in lung cancer diagnosis and treatment are discussed. With miR-199a as the core point and a divergence outward, the interplay between miR-199a and other ncRNAs is reviewed, and a regulatory network covering various cancers is depicted, which can help us to better understand the mechanism of cancer occurrence and provide a means for developing novel therapeutic strategies. In addition, the current methods of diagnosis and treatment of lung cancer are reviewed. Finally, a conclusion was drawn: miR-199a inhibits the development of lung cancer, especially by inhibiting the proliferation, infiltration, and migration of lung cancer cells, inhibiting tumor angiogenesis, increasing the apoptosis of lung cancer cells, and affecting the drug resistance of lung cancer cells. This review aims to provide new insights into lung cancer therapy and prevention.

The STING-IRF3 pathway contributes to paraquat-induced acute lung injury.

Immune and inflammatory responses play significant roles in paraquat (PQ)-induced acute lung injury (ALI), but the specific mechanisms remain unclear. Our study aimed to investigate the action of STING-IRF3 signaling on PQ-induced ALI in mice. Following PQ administration, samples were collected at 2, 12, 24, and 48 h for in vivo studies, and 24 h for in vitro studies. Following PQ administration (30 mg/kg, i.p.), injury to mouse lungs was evaluated by H&E staining and wet/dry ratios, and lung oxidative damage was evaluated by MDA and SOD assays. The mRNA levels of Sting, Irf3, and Ifnß were detected by RT-PCR, the expression of STING and IRF3 were assessed by western blotting and IHC/IF, and the secretion of IFNß was detected by ELISA. In vivo, PQ administration induced pathological changes and increased wet/dry ratios in lungs after 48 h. Sting, Irf3, and Ifnß mRNA levels in lung tissues, STING and pIRF3 protein levels in lung tissues, and IFNß secretion in serum, were upregulated by PQ in a time-dependent manner. PQ administration promoted IRF3 nuclear translocation in lung tissues after 48 h. The above changes were all attenuated by dexamethasone treatment (5 mg/kg, i.p., qd). In vitro, PQ induced STING and IRF3 translocation. Irf3 or Sting silencing decreased the mRNA levels and supernatant secretion of IFNß in PQ-treated RAW264.7 mouse macrophages. Sting silencing also inhibited the protein and mRNA levels of IRF3 in vitro. Our study suggests that STING-IRF3 signaling contributes to PQ-induced ALI, providing new information for future treatment strategies.

Management of high-risk breast lesions diagnosed on core biopsies and experiences from prospective high-risk breast lesion conferences at an academic institution.

BACKGROUND: The management of high-risk breast lesions diagnosed on image-guided core biopsy remains controversial. We implemented a high-risk breast conference attended by breast pathologists, imagers, and surgeons to prospectively review all contemporary cases in order to provide a consensus recommendation to either surgically excise or follow on imaging at 6-month intervals for a minimum of 2 years. METHODS: Between May, 2015 and June, 2019, 127 high-risk lesions were discussed. Of these 127 cases, 116 had concordant radiology-pathology (rad-path) findings. The remaining 11 patients had discordant rad-path findings. Of the 116 concordant cases, 6 were excluded due to lack of the first imaging follow-up until analysis. Of the remaining 110 patients, 43 had atypical ductal hyperplasia (ADH), 12 had lobular carcinoma in situ (LCIS), 19 had atypical lobular hyperplasia (ALH), 33 had radial scar (RS), 2 had flat epithelial atypia (FEA), and 1 had mucocele-like lesion (ML). We recommended excision for ADH if there were > 2 ADH foci or < 90% of the associated calcifications were removed. For patients with LCIS or ALH, we recommended excision if the LCIS or ALH was associated with microcalcifications or the LCIS was extensive. We recommended excision of RS when < 1/2 of the lesion was biopsied. We recommended all patients with FEA and ML for 6-month follow-up. RESULTS: Following conference-derived consensus for excision, of the 27 ADH excised, 9 were upgraded to invasive carcinoma or ductal carcinoma in situ. Of the six LCIS cases recommended for excision, none were upgraded. Nine excised radial scars revealed no upgrades. Additionally, 3 patients with ADH, 2 with ALH, 1 with LCIS, and 2 with RS underwent voluntary excision, and none were upgraded. All other patients (13 with ADH, 5 LCIS, 17 ALH, 22 RS, 2 FEA and 1 ML) were followed with imaging, and none revealed evidence of disease progression during follow-up (187-1389 days). All 11 rad-path discordant cases were excised with 2 upgraded to carcinoma. CONCLUSIONS: The results of this prospective study indicate that high-risk breast lesions can be successfully triaged to surgery versus observation following establishment of predefined firm guidelines and performance of rigorous rad-path correlation.

Downregulation of LINC01296 suppresses non-small-cell lung cancer via targeting miR-143-3p/ATG2B.

The 5-year survival rate of lung cancer is one of the lowest among various malignant tumors. Long noncoding RNAs (lncRNAs), noncoding RNAs longer than 200 nucleotides, can function either as tumor suppressors or as oncogenes. The aim of this study is to investigate the function of lncRNA LINC01296 and its molecular mechanism in non-small-cell lung cancer (NSCLC). According to the Gene Expression Omnibus database, 10 differentially expressed lncRNAs in NSCLC cells and patient tissues are upregulated. LINC01296 is the one with the most significant overexpression. Knockdown of LINC01296 inhibits the growth and migration, arrests the cell cycle, and promotes the apoptosis of NSCLC cells. Knocking down LINC01296 in vivo suppresses tumor growth and metastasis. LINC01296 also acts as the sponge of miR-143-3p. Lowering the expression of LINC01296 leads to decreased expression of autophagy-related 2B (ATG2B), a target gene of miR-143-3p. Moreover, downregulation of LINC01296 promotes paclitaxel sensitivity in NSCLC. These results demonstrated that the LINC01296/miR-143-3p/ATG2B axis is crucial in promoting the development of NSCLC and paclitaxel resistance. Our study may provide new ideas for the further research of clinical chemotherapy of NSCLC in the near future.

Roles of plant-derived bioactive compounds and related microRNAs in cancer therapy.

Plant-derived bioactive compounds, often called phytochemicals, are active substances extracted from different plants. These bioactive compounds can release therapeutic potential abilities via reducing antitumor drugs side effects or directly killing cancer cells, and others also can adjust cancer initiation and progression via regulating microRNAs (miRNAs) expression, and miRNA can regulate protein-coding expression by restraining translation or degrading target mRNA. A mass of research showed that plant-derived bioactive compounds including tanshinones, astragaloside IV, berberine, ginsenosides and matrine can inhibit tumor growth and metastasis by rescuing aberrant miRNAs expression, which has influence on tumor progression, microenvironment and drug resistance in multifarious cancers. This review aims to provide a novel understanding of plant-derived bioactive compounds targeting miRNAs and shed light on their future clinical applications.

Biochemical properties and progress in cancers of tRNA-derived fragments.

tRNA-derived small RNAs (tRFs), a kind of noncoding RNAs, are generated from transfer RNAs. tRFs have some types according to their source and sizes. They play important roles in cell life and carcinogenesis. In this paper, we review the biogenesis and biological properties. We also focus on current progress of tRFs and some tsRNAs such as tRF-Leu-CAG, which have been studied or will be further investigated in tumorgenesis and diagnostic biomarkers in the clinic.

Neonatal DEX exposure leads to hyperanxious and depressive-like behaviors as well as a persistent reduction of BDNF expression in developmental stages.

Brain-derived neurotrophic factor (BDNF), which regulates the neuronal survival, differentiation and synaptic plasticity, has been proved to play a critical role in the pathology and treatment of several psychiatric disorders including depression. Dexamethaone (DEX) is indicated for a number of conditions in perinatal medicine, however, the long-term impact of early-life DEX exposure on BDNF expression in hippocampus remains unknown. Here we found that neonatal DEX(ND) exposure leads to insignificant change of BDNF expression levels in the adulthood, albeit increased hyperanxious and depressive-like behaviors. However, the bdnf mRNA and BDNF protein levels were significantly reduced in all the hippocampal subregions during the developmental stages, including the perinatal period and puberty. We conclude that early life DEX exposure leads to a persistent disturbance of BDNF signaling during the developmental stages, which might be associated with the life-long impairment of hippocampal function.

Patients with benign papilloma diagnosed on core biopsies and concordant pathology-radiology findings can be followed: experiences from multi-specialty high-risk breast lesion conferences in an academic center.

BACKGROUND: To determine whether patients with benign papilloma diagnosed on core biopsy can be spared from surgery. METHODS: We prospectively reviewed 150 consecutive core biopsy-diagnosed papilloma cases at a multi-specialty high-risk breast lesion conference to determine whether surgical excision was necessary. Of these 150 cases, 148 had concordant radiologic-pathologic features. Six were excluded due to lack of the first imaging follow-up until analysis. 112 were benign papillomas; 17 were papillomas involved by atypical ductal hyperplasia (atypical papilloma); 6 papillomas had ADH in adjacent tissue but not involving the papilloma; 2 papillomas were involved by atypical lobular hyperplasia (ALH); and 5 papillomas had ALH in adjacent tissue. Two were radiology-pathology (rad-path) discordant. RESULTS: Thirty-nine of the 112 benign papillomas were excised with no upgrade to carcinoma; 73 were followed with no disease progression during follow-up (185-1279 days). Fifteen of 17 atypical papillomas were surgically excised with 4 (26.7%) upgraded to carcinoma. Four of the 6 patients with ADH adjacent to a benign papilloma underwent excision with 2 upgrades to carcinoma. None of the patients with papilloma, which was either involved by ALH or had ALH in adjacent tissue had upgrade or disease progression during follow-up (204-1159 days). Finally, the two cases with discordant path-rad discordant were excised with no upgrade. CONCLUSIONS: Our data confirm that rad-path concordant benign papillomas diagnosed on core biopsy do not require surgery. It also supports the value of a formal multi-specialty review of all benign papilloma cases to create a consensus management plan.

Quantitative digital imaging analysis of HER2 immunohistochemistry predicts the response to anti-HER2 neoadjuvant chemotherapy in HER2-positive breast carcinoma.

PURPOSE: Patients with HER2-positive breast cancer commonly receive anti-HER2 neoadjuvant chemotherapy and pathologic complete response (pCR) can be achieved in up to half of the patients. HER2 protein expression detected by immunohistochemistry (IHC) can be quantified using digital imaging analysis (DIA) as a value of membranous connectivity. We aimed to investigate the association HER2 IHC DIA quantitative results with response to anti-HER2 neoadjuvant chemotherapy. METHODS: Digitized HER2 IHC whole slide images were analyzed using Visiopharm HER2-CONNECT to obtain quantitative HER2 membranous connectivity from a cohort of 153 HER2+ invasive breast carcinoma cases treated with anti-HER2 neoadjuvant chemotherapy (NAC). HER2 connectivity and other factors including age, histologic grade, ER, PR, and HER2 fluorescence in situ hybridization (FISH) were analyzed for association with the response to anti-HER2 NAC. RESULTS: Eighty-three cases (54.2%) had pCR, while 70 (45.8%) showed residual tumor. Younger age, negative ER/PR, higher HER2 DIA connectivity, higher HER2 FISH ratio and copy number were significantly associated with pCR in univariate analysis. Multivariate analysis demonstrated only age, HER2 DIA connectivity, PR negativity, and HER2 copy number was significantly associated with pCR, whereas HER2 DIA connectivity had the strongest association. CONCLUSIONS: HER2 IHC DIA connectivity is the most important factor predicting pCR to anti-HER2 neoadjuvant chemotherapy in patients with HER2-positive breast cancer.

MicroRNA-1251-5p Promotes Carcinogenesis and Autophagy via Targeting the Tumor Suppressor TBCC in Ovarian Cancer Cells.

Accounting for more than 70% of ovarian cancer cases, epithelial ovarian malignancy has a low 5-year survival rate. MicroRNAs may be targeted in the clinical treatment of the disease. In this study, we first found that miR-1251-5p was significantly upregulated in human ovarian cancer cell lines and tissues with the cancer progression and stages. Overexpression or inhibition of miR-1251-5p promoted or impeded cell proliferation and cell cycle progression. Subsequently, TBCC, one of the tubulin-binding cofactors (TBCs), was identified as a target of miR-1251-5p to be negatively associated with cell cycle and autophagy. Exogenous overexpression of TBCC inhibited the expressions of CDK4 and LC3BII, but it promoted the expressions of α/ß-tubulin and p62 to suppress cell growth and autophagy, particularly under the starving condition; whereas the introduction of miR-1251-5p in TBCC-overexpressing cells rescued the suppressive effects of TBCC on cell cycle and autophagy through the inverse regulation of the above proteins. Finally, miR-1251-5p was proven to enhance xenograft tumor growth through the downregulation of TBCC but upregulation of Ki67 and LC3B in xenograft tumor tissues. Collectively, these results suggest that miR-1251-5p functions as an oncogene to suppress TBCC and α/ß-tubulin expression. Thus, the miR-1251-5p/TBCC/α/ß-tubulin axis may be targeted for ovarian cancer treatment.

Mechanical and Thermal Properties of Polyether Polytriazole Elastomers Formed by Click-Chemical Reaction Curing Glycidyl Azide Polymer.

Energetic binders are a research hot-spot, and much emphasis has been placed on their mechanical properties. In this study, propargyl-terminated ethylene oxide-tetrahydrofuran copolymer (PTPET) was synthesized. Then, PTPET and low-molecular-weight ester-terminated glycidyl azide polymer (GAP) were reacted by the click reaction without using catalysts to obtain a polyether polytriazole elastomer. Through tensile tests, where R = 0.5, the tensile strength reached 0.332 MPa, with an elongation at break of 897.1%. Swelling tests were used to measure the cross-linked network and showed that the cross-linked network regularity was reduced as R increased. The same conclusions were confirmed by dynamic mechanical analysis (DMA). In DMA curves, Tg was around -70 to -65 °C, and a small amount of crystallization appeared at between -50 and -30 °C, because locally ordered structures were also present in random copolymers, thereby forming localized crystals. Their thermal performance was tested by Differential Scanning Calorimeter (DSC) and Thermal Gravimetric Analyzer (TG), and the main mass loss occurred at around 350 to 450 °C, which meant that they were stable. In conclusion, the polyether polytriazole elastomer can be used as a binder in a composite propellant.

MicroRNA-296-5p promotes healing of diabetic wound by targeting sodium-glucose transporter 2 (SGLT2).

BACKGROUND: Diabetic wounds are refractory and very difficult to heal. We aimed to use miRNA to identify novel and specific molecular markers for diabetes mellitus (DM) diagnosis and treatment. METHODS: The expression level of miR-296-5p was determined in tissue samples of 12 DM patients. The effect of miR-296-5p on proliferation of ß-cells was examined using Cell Counting Kit-8 (CCK-8) and colony formation assay. The effect of miR-296-5p on cell cycle progression was analysed using flow cytometry. The target gene was verified using luciferase reporter assay. A rat diabetes model was used to assess the effect of miR-296-5p in vivo. RESULTS: Overexpression of miR-296-5p suppressed cell proliferation, arrested cell cycle progression, and increased the healing rate of diabetic wounds both in vivo and in vitro. TargetScan analysis results showed that miR-296-5p is a direct regulator of SGLT2. CONCLUSIONS: miR-296-5p can increase the healing rate of diabetic wounds and may be an effective molecular tool in DM diagnosis and therapy.

Rapamycin- and starvation-induced autophagy are associated with miRNA dysregulation in A549 cells.

MicroRNAs (miRNAs) are short (20-23 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. In recent years, deep sequencing of the transcription is being increasingly utilized with the promise of higher sensitivity for the identification of differential expression patterns as well as the opportunity to discover new transcripts, including new alternative isoforms and miRNAs. In this study, miRNAs from A549 cells treated with/without rapamycin or starvation were subject to genome-wide deep sequencing. A total of 1534 miRNAs were detected from the rapamycin- and starvation-treated A549 cells. Among them, 31 miRNAs were consistently upregulated and 131 miRNAs were downregulated in the treated cells when compared with the untreated cells. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis of the predicted target genes of the most significantly differentially expressed miRNAs revealed that the autophagy-related miRNAs are involved in cancer pathway. Taken together, our findings indicate that the underlying mechanism responsible for autophagy is associated with dysregulation of miRNAs in rapamycin- or starvation-induced A549 cells.

Functional role of RRS1 in breast cancer cell proliferation.

RRS1 (human regulator of ribosome synthesis 1), an essential nuclear protein involved in ribosome biogenesis, is overexpressed in some human cancers, yet its role in breast cancer remains unclear. Here, we report a functional analysis of RRS1 in breast cancer and its likely mechanism. Immunohistochemistry (IHC) and RT-qPCR analyses indicated that RRS1 was commonly overexpressed in breast cancer tissues. The copy numbers of RRS1 were higher in tumours compared with those for normal tissues. And there was a significant correlation between copy number and mRNA expression. In addition, RRS1 overexpression was significantly correlated with lymph node metastasis and poor survival. RRS1 mRNA and protein levels were also significantly increased in a panel of human breast cancer cell lines. RRS1 knockdown inhibited proliferation and induced apoptosis and cell cycle arrest in all three cell lines. Furthermore, RRS1 knockdown suppressed the tumour formation and growth of MDA-MB-231 cells in nude mice. Additionally, RRS1 knockdown activated p53 and p21 in MCF-7 cells. A marked increase in the quantity of ribosome-free RPL11 was detected by Western blot. Moreover, co-immunoprecipitation (CoIP) experiments showed that RRS1 knockdown activated p53 by facilitating the direct contact of MDM2 and RPL11/RPL5. Taken together, our results suggest that RRS1 may contribute to breast cancer proliferation through RPL11/MDM2-mediated p53 activation. Therefore, RRS1 may be a promising target for breast cancer therapy.

Biology of MiR-17-92 Cluster and Its Progress in Lung Cancer.

MicroRNAs, a class of short endogenous RNAs, acting as post-transcriptional regulators of gene expression, mostly silence gene expression via binding imperfectly matched sequences in the 3'UTR of target mRNA. MiR-17-92, a highly conserved gene cluster, has 6 members including miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1 and miR-92a. The miR-17-92 cluster, regarded as oncogene, is overexpressed in human cancers. Lung cancer is the leading cause of death all over the world. The molecular mechanism of lung cancer has been partly known at the levels of genes and proteins in last decade. However, new prognosis biomarkers and more target drugs should be developed in future. Therefore, noncoding RNAs, especially miRNAs, make them as new potentially clinical biomarkers for diagnosis and prognosis. In this review, we focus the current progress of miR-17-92 cluster in lung cancer.