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Excessive drinking is one of the main causes of liver cancer. In the process of alcohol metabolism, aldehyde dehydrogenase 2 (ALDH2) is the key enzyme of acetaldehyde metabolism. ALDH2 gene deficiency is positively associated with the risk of hepatocellular carcinoma (HCC). However, no studies have shown a connection between ALDH2 and another metabolic regulatory gene, SLC3A2. In this study, we analyzed the expression levels of ALDH2 and SLC3A2 in liver cancer tissues based on the TCGA database. Subsequently, we constructed ALDH2 knockout and SLC3A2 knock-in transgenic mice to check the roles of ALDH2 and SLC3A2 in tumorigenesis in vivo. In addition, we examined the mechanisms of ALDH2 and SLC3A2 in HCC cells using small RNA interference technology. Consistent with previous studies, we also confirmed the functions of ALDH2 in inhibiting hepatocarcinogenesis, while SLC3A2 had the opposite effect. The main finding of this study is that ALDH2 inhibited BSG expression through the TGF-ß1 pathway, which indirectly inhibited SLC3A2 expression; subsequently, the sphingolipid metabolism pathway was also inhibited in HCC cells. Therefore, SLC3A2 is a novel target for HCC treatment.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Camundongos , Animais , Neoplasias Hepáticas/genética , Carcinoma Hepatocelular/patologia , Aldeído-Desidrogenase Mitocondrial/genética , Aldeído-Desidrogenase Mitocondrial/metabolismo , Etanol/metabolismo , Camundongos Transgênicos , Esfingolipídeos , Aldeído Desidrogenase/genética , Aldeído Desidrogenase/metabolismo , Acetaldeído/metabolismoRESUMO
Different ethnic groups have different incidence rate of hepatocellular carcinoma (HCC). In addition to lifestyle and environmental factors, genetic susceptibility is also an important reason. In this study, we screened the immune related genes and stromal related genes in White and Asian liver cancer patients cohort of The Cancer Genome Atlas (TCGA) the using ESTIMATE algorithm. Hub genes that significantly associated with overall survival (OS) were selected from White and Asian liver cancer patients, respectively. In addition, we validated the functions of two hub genes, IL-18RAP and GPM6A, in vivo and in vitro. We confirmed different races have different tumor immune microenvironments. Immune microenvironment can influence and change the efficacy of immunotherapy for liver cancer patients.
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Cancer stem cells (CSCs) are a subset of cancer cells with stem cell characteristics. The discovery of CSCs has opened a new era for cancer research. CSCs not only play a critical role in tumorigenesis, but also are responsible for the failure of cancer treatments. Here, we performed weighted gene co-expression network analysis (WGCNA) to identify key stemness genes and prognostic signatures using the data of an Asian liver cancer patient cohort and a White liver cancer patient cohort in The Cancer Genome Atlas (TCGA) database. To compare the difference in tumorigenesis between the Asian patients and the White patients, the prognostic value of the key genes from the Asian patients was evaluated in the White patient cohort and vice versa. We found that some key genes could predict the survival of the patients regardless of race. In addition, the key genes, NUCB2 and KLF4A, were selected from Asian patients and White patients, respectively, for further experimental validation. Knocking down NUCB2 could inhibit the activity of the AKT/mTOR signaling pathway and reverse the epithelial-mesenchymal transition (EMT) in liver cancer cells. We also confirmed that the knockdown of KLF4A suppressed ABCG2 activity and reduced the side population (SP) in liver cancer cells for the first time. Our results suggest that the stemness index is a useful method to identify key genes in tumorigenesis. Compared to the analysis for all patients, applying this index to the analysis of the patients of different races will provide more potential therapeutic targets for cancer treatment.
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BACKGROUND: Liver cancer seriously threatens human health. Natural killer (NK) cells are an important part of the innate immune system and have strong anti-tumor ability. Immunotherapy based on NK cells has become a hot topic in the treatment of liver cancer. METHODS: In this study, we checked the serum DKK3 (sDKK3) and circulating CD56bright NK cells using ELISA and flow cytometry, respectively, in the blood of liver cancer patients. The effect on recombinant human DKK3 (rhDKK3) on CD56bright NK cells was analyzed in vitro. RESULTS: We found low levels of sDKK3 in liver cancer patients and a negative correlation between sDKK3 and circulating CD56bright NK cells. In addition, we found that DKK3 induced the differentiation and improved the cytotoxicity of CD56bright NK cells for the first time. It could be used as an agonist for NK cell-based immunotherapy. CONCLUSIONS: Improving the clinical efficacy of NK cells through DKK3 will become a new strategy for cancer immunotherapy.
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Células Matadoras Naturais , Neoplasias Hepáticas , Humanos , Antígeno CD56 , Células Matadoras Naturais/metabolismo , Células Matadoras Naturais/patologia , Neoplasias Hepáticas/terapia , Neoplasias Hepáticas/patologia , Citometria de Fluxo , Diferenciação Celular , Proteínas Adaptadoras de Transdução de SinalRESUMO
Malignant tumors seriously endanger human health and life, and restrict economic development. Human leukocyte antigen (HLA) is the expression product of the human major histocompatibility complex, which, at present, is the most complex known polymorphic system. The polymorphism and expression of HLA molecules have been demonstrated to be associated with the occurrence and development of tumors. HLA molecules can regulate the proliferation of tumor cells and inhibit antitumor immunity. In the present review, the structure and function of HLA molecules, the polymorphism and expression of HLA in tumor tissue, the roles of HLA in tumor cells and tumor immunity, and the potential clinical application of HLA in tumor immunotherapy are summarized. The overall aim of the present review is to provide relevant information for the development of antitumor immunotherapies involving HLA in the clinic.
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Antígenos de Histocompatibilidade Classe I , Neoplasias , Humanos , Antígenos de Histocompatibilidade Classe I/genética , Antígenos HLA/genética , Neoplasias/genética , Neoplasias/terapia , Antígenos de Histocompatibilidade Classe II , ImunoterapiaRESUMO
In this review, we discussed an interesting case infected with "COVID-19" (Corona Virus Disease 2019). The patients with Hodgkin's lymphoma recovered after infection with COVID-19. It may be that COVID-19 activates the patient's immune system, or it may be a coincidence. COVID-19 spike protein can interact with CD147 and use it as an entry to invade host cells. CD147 is a partner of SLC3A2, which is the chaperone subunit of cystine/glutamate reverse transporter (system XC). The catalytic subunit of system XC is SLC7A11. SLC7A11 mediated cysteine uptake plays a key role in ferroptosis. Through literature review and data analysis, we suggest that CD147, as a new potential COVID-19 infection entry, may also lead to ferroptosis of host cells. Our hypothesis is that spike protein of COVID-19 induced ferroptosis in host cells via CD147/SLC3A2/SLC7A11 complex. This is another explanation for the cancer patient recovered after COVID-19 infection.
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COVID-19 , Neoplasias , Humanos , Glicoproteína da Espícula de Coronavírus , Análise de Dados , Neoplasias/complicaçõesRESUMO
Most patients with liver cancer were found late and lost the chance of surgery. Liquid biopsy can monitor the risk of tumor recurrence and metastasis, quickly evaluate the curative effect of tumor treatment, and is conducive to early screening and auxiliary diagnosis of high-risk groups. Amino acid (AA) profiling has been used to the diagnosis and the prognosis for cancers. However, little was known about the profiles of AA of liver cancer. In this study, we used tRNA in Cancer database to analyze the AA levels in liver cancer tissues. Blood samples of patients with liver cancer were collected and analyzed using the automatic AA analyzer. We found that valine, isoleucine, and leucine were decreased significantly both in the plasma and the tumor tissues of patients with liver cancer. However, upregulation of methionine was observed in tissues and plasma of patients with liver cancer. Interestingly, tyrosine, and phenylalanine were decreased in tumor tissue but increased in the plasma of patients with liver cancer. This is the first report provided an overview of AA profile in both plasma and tissue for patients with liver cancer. AA levels can be used as diagnostic and prognostic markers of patients with liver cancer.
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SLC3A2, the heavy chain of the CD98 protein, is highly expressed in many cancers, including lung cancer. It can regulate the proliferation and the metastasis of cancer cells via the integrin signaling pathway. Liquid biopsy is a novel method for tumor diagnosis. The diagnostic or prognostic roles of serum SLC3A2 in lung cancer are still not clear. In this study, we analyzed SLC3A2 mRNA levels in human lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) using the TCGA database and serum SLC3A2 protein levels using ELISA. We confirmed high SLC3A2 levels in both the serum and tissue of LUAD and LUSC patients. Both serum and tissue SLC3A2 could be used as prognostic markers for overall LUAD and subgroups of LUSC patients. SLC3A2 induced tumorigenesis via the MEK/ERK signaling pathway in LUAD and LUSC cells.
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BACKGROUND: Molecule interacting with CasL-like protein 2 (MICALL2) is believed to regulate cytoskeleton dynamics, tight junction formation, and neurite outgrowth. However, its biological role and the underlying mechanism in colorectal cancer (CRC) remain largely elusive. METHODS: qRT-PCR, Western blotting and immunohistochemistry assays were used to detect the expression levels of different genes. Next, mass spectrometry, co-immunoprecipitation and immunofluorescence staining were used to detect the interactions of proteins. Furthermore, MTT assay, colony formation assay, wound-healing assays and xenograft tumor models were performed to demonstrate the functions of MICALL2 in CRC. In addition, transcriptome sequencing and Western blotting were conducted to verify the mechanism of MICALL2 in CRC. RESULTS: We found that both mRNA and protein levels of MICALL2 are up-regulated in colorectal cancer tissues compared with non-tumor tissues and that its overexpression is closely correlated with poor prognosis. Ubiquitin E3 ligase Tripartite motif-containing protein 21 (TRIM21) mediated MICALL2 ubiquitination and proteasome-dependent degradation, negatively correlated with MICALL2 levels, and reversely regulated the tumorigenic activity of MICALL2 in CRC. Functional studies confirmed that MICALL2 promoted colorectal cancer cell growth and migration via the Wnt/ß-catenin signaling pathway. CONCLUSIONS: As a substrate of ubiquitinase TRIM21, MICALL2 enhances the growth and migration of colorectal cancer cells and activates the Wnt/ß-catenin signaling pathway. Video abstract.
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Neoplasias Colorretais , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Colorretais/patologia , Via de Sinalização Wnt/genética , Carcinogênese/genética , Transformação Celular Neoplásica , Proliferação de Células , Linhagem Celular Tumoral , beta Catenina/metabolismo , Movimento Celular/genéticaRESUMO
Cancer stem cell (CSC) refers to cancer cells with stem cell properties, that is, they have the ability of "self-renewal" and "differentiation." Cancer stem cells exist in cancer cells and are the "culprit" of cancer recurrence and metastasis. It is difficult to be found because of its small amount, and it is difficult for anticancer drugs to produce effects on it. At present, the isolation and identification of cancer stem cells from many solid tumors are still quite difficult, mainly due to the lack of specific molecular markers of cancer stem cells. In this review, cancer stem cell surface markers and functional markers in urinary system were summarized. These markers can provide molecular targets for cancer therapy.
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Cancer stem cells (CSC) theory has ushered in a new era of cancer research. Tumor recurrence, metastasis and chemotherapy resistance are all related to the existence of cancer stem cells. Further understanding of tumor heterogeneity will contribute to targeted treatment. Liver cancer and pancreatic cancer are common digestive gland tumors with high lethality. This article reviews the identification and isolation of CSC markers in hepatocellular carcinoma and pancreatic cancer. The markers related signal pathways are involved in the occurrence and development of tumors, and have a significant impact on the proliferation, metastasis and invasion of cancer cells, which can be used as potential molecular therapeutic targets. This study will be helpful to understand cancer stem cell like cells.
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Neoplasias Hepáticas , Neoplasias Pancreáticas , Biomarcadores Tumorais/metabolismo , Humanos , Recidiva Local de Neoplasia/patologia , Células-Tronco Neoplásicas/metabolismo , Neoplasias Pancreáticas/metabolismo , Neoplasias PancreáticasRESUMO
Exposure to high doses of anticancer drugs can induce the emergence of a subpopulation of weakly proliferative and drug-tolerant cells. Drug tolerance can reduce the benefits obtained from canonical treatment and reduce the survival rate of patients. Regulation of SRY-related HMG box transcription factor 4 (SOX4) has been proved to affect drug sensitivity. The current study aimed to explore the role of SOX4 in drug resistance of colorectal cancer (CRC) cells as well as the related molecular mechanisms. Expression patterns of SOX4, microRNA-17 (miR-17), and CYLD in both CRC tissues and cells were determined with their relationship analyzed by bioinformatics analysis, dual-luciferase reporter gene assay, and ChIP. Loss- and gain-function assays were performed to ascertain the effect of SOX4, miR-17, and CYLD on biological cellular processes and drug resistance to 5-FU. SOX4 and miR-17 were found to be highly expressed while CYLD was poorly expressed in CRC tissues and cells. Silencing of SOX4 resulted in the suppression of cellular proliferation, invasion, migration as well as a reduction in CRC drug resistance. Mechanically, CYLD was specifically targeted by miR-17, while SOX4 upregulated the expression of miR-17. Functionally, SOX4 triggered drug resistance of CRC cells to 5-FU through the miR-17/CYLD axis. Taken together, the key findings of the present study provides evidence suggesting that SOX4 elevates miR-17 to decrease CYLD, thus inducing chemotherapy resistance of CRC cells.
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Neoplasias Colorretais/metabolismo , Enzima Desubiquitinante CYLD/biossíntese , Regulação para Baixo , Regulação Enzimológica da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , MicroRNAs/biossíntese , RNA Neoplásico/biossíntese , Fatores de Transcrição SOXC/metabolismo , Ativação Transcricional , Animais , Linhagem Celular Tumoral , Neoplasias Colorretais/genética , Enzima Desubiquitinante CYLD/genética , Feminino , Humanos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/genética , RNA Neoplásico/genética , Fatores de Transcrição SOXC/genéticaRESUMO
MICAL1 has been reported to be involved in the malignant processes of several types of cancer cells, however, the roles of MICAL1 in colorectal cancer (CRC) have not been well-characterized. This study aims to investigate the cellular functions and molecular mechanisms of MICAL1 in CRC cells. Here, we found that both mRNA and protein levels of MICAL1 were down-regulated in colorectal cancer tissues compared with matched adjacent non-tumor tissues, and the expression level of MICAL1 was correlated with the metastatic status of colorectal cancer. Importantly, overexpression of MICAL1 significantly inhibited colorectal cancer cell migration and growth, and increased the level of E-cadherin and Occludin, and suppressed the expression level of Vimentin and N-cadherin; while silencing of MICAL1 promoted CRC cell migration and enhanced EMT. In addition, MICAL1 overexpression significantly inhibited the proliferation and growth of CRC in vitro and in vivo. Moreover, RNA sequencing and bioinformatics analysis identified that MICAL1 was closely correlated with "cell migration", "cell cycle" and "ß-catenin signaling" genesets. Mechanistically, overexpression of MICAL1 downregulated the mRNA level of EGR1 and ß-catenin, decreased the protein level and nuclear translocation of ß-catenin, and inhibited the transcriptions of ß-catenin downstream targets, c-myc and cyclin D1. The ectopic expression of EGR1 or ß-catenin can significantly block the MICAL1-mediated inhibitory effects. Collectively, MICAL1 is down-regulated in CRC, and plays an inhibitory role in the migration and growth of CRC cells by suppressing the ERG1/ß-catenin signaling pathway.
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Movimento Celular/genética , Proliferação de Células/genética , Neoplasias Colorretais/genética , Proteína 1 de Resposta de Crescimento Precoce/genética , Proteínas dos Microfilamentos/genética , Oxigenases de Função Mista/genética , Transdução de Sinais/genética , beta Catenina/genética , Animais , Caderinas/genética , Caderinas/metabolismo , Linhagem Celular Tumoral , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/patologia , Proteína 1 de Resposta de Crescimento Precoce/metabolismo , Transição Epitelial-Mesenquimal/genética , Feminino , Regulação Neoplásica da Expressão Gênica , Células HCT116 , Humanos , Camundongos Endogâmicos BALB C , Camundongos Nus , Proteínas dos Microfilamentos/metabolismo , Oxigenases de Função Mista/metabolismo , Transplante Heterólogo , Carga Tumoral/efeitos dos fármacos , beta Catenina/metabolismoRESUMO
MiR-328-3p has been reported to be downregulated and serve as a tumor suppressor in several cancers. Previous studies only have reported the downregulation of miR-328-3p in CRC. However, the roles of miR-328-3p in CRC growth and metastasis were unknown. In this study, we demonstrated that miR-328-3p overexpression inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). The PI3K/Akt signaling pathway was also inactivated by miR-328-3p overexpression. MiR-328-3p knockdown showed the opposite effects. In addition, we confirmed that miR-328-3p directly bound to 3'UTR of Girdin and negatively regulated its expression. Girdin knockdown or treatment with PI3K inhibitor LY294002 blocked the effects of miR-328-3p inhibitor on cell proliferation, metastasis, and the PI3K/Akt signaling pathway. Moreover, pre-miR-328 decreased numbers of liver metastatic nodules, and reduced the levels of p-Akt, p-Girdin, and Girdin in metastatic tissues in liver. In conclusion, miR-328-3p may inhibit proliferation and metastasis of CRC cells by targeting Girdin and inactivating the PI3K/Akt signaling pathway. MiR-328-3p may be a novel target in cancer therapy.
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Proliferação de Células , Neoplasias Colorretais/genética , MicroRNAs/metabolismo , Proteínas dos Microfilamentos/genética , Proteínas de Transporte Vesicular/genética , Animais , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/patologia , Transição Epitelial-Mesenquimal , Células HCT116 , Humanos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/genética , Proteínas dos Microfilamentos/metabolismo , Metástase Neoplásica , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Proteínas de Transporte Vesicular/metabolismoRESUMO
MiR-346-5p is overexpressed in several cancers, including colorectal cancer (CRC). However, the effects of miR-346-5p on CRC progression have not yet been clarified. In our study, miR-346-5p levels in four CRC cell lines and normal human colon epithelial cells were determined by real-time PCR. SW620 and HCT116 cells were selected and then transfected with miR-346-5p mimic, miR-346-5p inhibitor, or specific siRNAs targeting F-box/LRR-repeat protein 2 (FBXL2). Cell proliferation, cell cycle distribution and cell cycle regulators were examined by CCK-8 assay, flow cytometry, and western blot. The binding of miR-346-5p on 3' untranslated region (UTR) of FBXL2 were verified by dual-luciferase reporter assay. CRC cells were co-transfected with miR-346-5p inhibitor and siFBXL2 to investigate the involvement of FBXL2. Interaction of FBXL2 with forkhead box M1 (FoxM1) was examined by co-immunoprecipitation (Co-IP) assay. The effect of miR-346-5p knockdown on CRC tumorigenesis in vivo was investigated. Here, we found that miR-346-5p overexpression promoted, while miR-346-5p knockdown inhibited cell proliferation and G1-S transition. Inhibition of FBXL2 showed similar effects as miR-346-5p overexpression. Moreover, we verified that FBXL2 was a direct target of miR-346-5p. FBXL2 interacted with FoxM1, and then negatively regulated both FoxM1 and nuclear ß-catenin levels. Additionally, FBXL2 knockdown reversed the effects of miR-346-5p inhibitor. In xenograft models, miR-346-5p knockdown significantly inhibited tumor growth, increased FBXL2 expression, and downregulated the levels of FoxM1 and nuclear ß-catenin. In conclusion, miR-346-5p may promote CRC growth by targeting FBXL2 and activating the ß-catenin signaling pathway. MiR-346-5p may be a novel target in cancer therapy.
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Neoplasias Colorretais/metabolismo , Proteínas F-Box/metabolismo , MicroRNAs/genética , Animais , Apoptose/genética , Carcinogênese/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Neoplasias Colorretais/genética , Proteínas F-Box/genética , Proteína Forkhead Box M1/metabolismo , Pontos de Checagem da Fase G1 do Ciclo Celular/genética , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/metabolismo , Transdução de Sinais/genética , Via de Sinalização Wnt/genética , Ensaios Antitumorais Modelo de Xenoenxerto , beta Catenina/metabolismoRESUMO
BACKGROUND/AIM: Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL)-based therapies have been used in many human cancers. However, some tumors are resistant to TRAIL-induced cell death. Aldehyde dehydrogenase 1 (ALDH1) is a functional marker for identification of CSCs. METHODS: In this study, we used the colony formation assay, AnnexinV/ PI double staining and PI staining to detect proliferation, apoptosis and cell cycle in ALDH1+ non-small cell lung cancer (NSCLC) cells with TRAIL treatment. In addition, we established xenograft mouse models to confirm the anti-tumor roles of TRAIL in vivo. Finally, gene array and western blot were used to detect the deeper mechanism of the susceptibility of ALDH1+ NSCLC cells to TRAIL. RESULTS: We confirmed that TRAIL could inhibit proliferation, and induce apoptosis and G1 arrest in ALDH1+ NSCLC cells. Correspondingly, TRAIL was associated with decreased tumor size and the favorable survival rate of ALDH1+ cells established xenograft mouse models. ALDH1 could increase the death receptors (DR) 4 and DR5 expression in ALDH1+ NSCLC cells via activating MEK/ERK signaling pathway. CONCLUSION: ALDH1 protein induced MEK-1 mRNA stability and promoted its translation via its 3'UTR.
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Isoenzimas/metabolismo , MAP Quinase Quinase 1/metabolismo , Retinal Desidrogenase/metabolismo , Regiões 3' não Traduzidas , Família Aldeído Desidrogenase 1 , Animais , Apoptose/efeitos dos fármacos , Sítios de Ligação , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/mortalidade , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral , Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos , Humanos , Isoenzimas/química , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/patologia , MAP Quinase Quinase 1/antagonistas & inibidores , MAP Quinase Quinase 1/genética , Camundongos , Camundongos Endogâmicos NOD , Camundongos SCID , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo , Retinal Desidrogenase/química , Transdução de Sinais/efeitos dos fármacos , Taxa de Sobrevida , Ligante Indutor de Apoptose Relacionado a TNF/farmacologia , Ligante Indutor de Apoptose Relacionado a TNF/uso terapêuticoRESUMO
Cluster of ddifferentiation 24 (CD24) is a widely used cancer stem cell (CSC) marker in numerous cancer types. However, a number of studies have shown that CD24 is a prognostic marker, but not a CSC marker for lung adenocarcinoma. In the present study, firstly, bioinformatic analyses were used to identify the CD24 mRNA levels in the subtypes of lung cancer. Secondly, CD24high and CD24low cells were isolated from the side population of Lewis lung carcinoma (LLC) cells using flow cytometry. Furthermore, the stemness of CD24high and CD24low cells were determined in vivo and in vitro. Lastly, the mechanism(s) of nicotine-inhibited CD24 expression in LLC cells were assessed. The main findings of this study are that: i) CD24 could be used as a prognostic marker for human lung adenocarcinoma; ii) the in vitro and in vivo experiments did not determine a significant influence of CD24 on the tumorgenicity of LLC cells; and iii) nicotine inhibited CD24 expression in LLC cells by upregulation of RAS. However, the detailed mechanism(s) of these results require further analysis.
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Antígeno CD24/genética , Carcinoma Pulmonar de Lewis/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Nicotina/administração & dosagem , Proteínas ras/metabolismo , Animais , Biomarcadores Tumorais/antagonistas & inibidores , Biomarcadores Tumorais/genética , Antígeno CD24/antagonistas & inibidores , Antígeno CD24/metabolismo , Carcinoma Pulmonar de Lewis/genética , Carcinoma Pulmonar de Lewis/metabolismo , Carcinoma Pulmonar de Lewis/patologia , Linhagem Celular Tumoral , Feminino , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Camundongos , Células-Tronco Neoplásicas/metabolismo , Nicotina/farmacologia , Prognóstico , Análise de Sobrevida , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
OBJECTIVES: To explore and evaluate a sexually transmitted disease (STD)/HIV intervention program targeting female sex workers working in entertainment establishments in five different settings in China. DESIGN AND METHOD: A prospective, community-based, pre/post, intervention trial set in entertainment establishments (karaoke bars, massage parlours, dance halls, beauty parlours) where sex workers operate at sites in five provinces of China: Anhui, Beijing, Fujian, Guangxi and Xinjiang. The participants were all sex workers working in targeted entertainment establishments. A Women's Health Clinic was set up near participants' places of work at each site. Clinic-based outreach activities, including awareness-raising, condom promotion, and sexual health care, were developed and delivered to sex workers. Cross-sectional surveys at baseline and post-intervention were used to evaluate changes in condom use with the last three clients, and the prevalence of chlamydia and gonorrhoea. RESULTS: In total, 907 sex workers were surveyed at baseline and 782 at 12 months post-intervention. Outreach teams made 2552 visits to the target entertainment establishments, approached 13,785 female sex workers, and distributed 33,575 copies of education material and 5102 packets of condoms. The rate of condom use with the most recent three clients increased from 55.2% at baseline to 67.5% at 12 months evaluation. The prevalence of gonorrhoea fell from 26% at baseline to 4% after intervention, and that of chlamydia fell from about 41 to 26%. CONCLUSION: The intervention was effective for increasing condom use and reducing STD among sex workers. The results were used to develop national guidelines on sex worker interventions for nationwide scale up.