ABSTRACT
The Late Triassic Carnian Pluvial Episode (CPE) witnessed enormous climate change closely associated with volcanic activity. However, the coupling relationship between volcanic activity and climate change, which may be linked to chemical weathering, has not yet been fully uncovered. We used lithium contents and isotopes of volcanic ash (VA)-bearing lacustrine shale to constrain their deposition pathways and response to climate changes, i.e., weathering intensity, during the Late Triassic era. Elevated δ7Li (i.e., >2.5) and low Li contents (i.e., <65 microgram per gram) in shale likely document the direct depositing of volcanic lithium from airborne VA, which mainly inherited Earth's interior δ7Li signal. By contrast, shale yields markedly high lithium contents (i.e., >135 microgram per gram), alongside relatively low δ7Li (i.e., <0), likely implying waterborne VA dominated by intensified weathering under a super humidity climate. Hence, this study provides evidence for the differential VA-rich shale deposition model related to chemical weathering states synchronous with climate changes during the CPE period.
ABSTRACT
Earth has a prolonged history characterized by substantial cycling of matter and energy between multiple spheres. The production of organic carbon can be traced back to as early as â¼4.0 Ga, but the frequency and scale of organic-rich shales have varied markedly over geological time. In this paper, we discuss the organic carbon cycle and the development of black shale from the perspective of Earth System Science. We propose that black shale depositions are the results of interactions among lithospheric evolution, orbital forcing, weathering, photosynthesis and degradation. Black shales can record Earth's oxygenation process, provide petroleum and metallic mineral resources and reveal information about the driver, direction and magnitude of climate change. Future research on black shales should be expanded to encompass a more extensive and more multidimensional perspective.
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High metastatic potential and resistance to immunotherapy lead to poor survival in patients with ovarian cancer. Angiopoietin-like protein 3 is aberrantly expressed and exerts diverse roles in the progression of several cancers. However, its function in ovarian cancer is unknown. Here, decreased expression of angiopoietin-like protein 3 was observed in ovarian cancer tissues and cells. Moreover, patients with high expression of angiopoietin-like protein 3 had longer overall survival and progression-free survival, indicating a good prognosis for patients. Furthermore, angiopoietin-like protein 3 overexpression inhibited ovarian cancer cell proliferation. Concomitantly, high invasion and the occurrence of epithelial-to-mesenchymal transition of cancer cells were restrained after angiopoietin-like protein 3 elevation. Up-regulation of angiopoietin-like protein 3 expression further increased interleukin 2-treated natural killer cell activation by increasing CD69 expression and production of interferon gamma and tumor necrosis factor-alpha when natural killer cells were co-cultured with ovarian cancer cells. Importantly, angiopoietin-like protein 3 overexpression enhanced natural killer cell-evoked cytotoxicity and apoptosis of cancer cells, indicating the pro-tumor killing ability of angiopoietin-like protein 3 for natural killer cells. Mechanistically, angiopoietin-like protein 3 elevation inhibited activation of the Janus Kinase/Signal transducer and activator of transcription 3 signaling in ovarian cancer cells by inhibiting protein expression of phospho-Janus Kinase 2, phospho-Signal transducer and activator of transcription 3, downstream matrix metallopeptidase 2 and programmed cell death 1. Moreover, blocking the Janus Kinase/Signal transducer and activator of transcription 3 pathway via their inhibitor Stattic restrained ovarian cancer cell proliferation, invasion, epithelial-to-mesenchymal transition, and promoted natural killer cell killing to ovarian cancer cells. Thus, these findings reveal that angiopoietin-like protein 3 may act as an anti-oncogenic regulator to inhibit the metastatic potential and enhance the susceptibility of ovarian cancer cells to natural killer cell-mediated killing. Consequently, angiopoietin-like protein 3 may regulate metastatic potential and immune escape from natural killer cells, indicating a promising therapeutic strategy for ovarian cancer.
ABSTRACT
The Jurassic shale in the northeastern Sichuan Basin is one of the main target intervals for continental shale gas exploitation. Research on the pore structure and gas-bearing properties of shales is the key issue in target interval optimization. Through core observation, geochemistry, bulk minerals, scanning electron microscopy, nitrogen adsorption, and isothermal adsorption experiments, various lithofacies with different pore structure characteristics were clarified. In addition, the factors that control gas-bearing properties were discussed, and a continental shale gas enrichment model was finally established. The results show that the Jurassic continental shale in the northeastern Sichuan Basin can be classified into six lithofacies. Organic pores, intergranular pores, interlayer pores in clay minerals, intercrystalline pores in pyrite framboids, and dissolution pores can be observed in shale samples. Pore structures varied in different shale lithofacies. The contact angle of shales is commonly less than 45°, leading to complex wettability of pores in the shales. Free gas content is mainly controlled by the organic matter (OM) content and the brittleness in the Jurassic shale. The adsorbed gas content is mainly controlled by the OM content, clay mineral type, and water saturation of the shales. The enrichment mode of the Lower Jurassic continental shale gas in the northeastern Sichuan Basin is established. Paleoenvironments control the formation of organic-rich shales in the center part of lakes. The "baffle" layer helps the confinement and high pressure, and the complex syncline controls the preservation, forming the enrichment pattern of the complex syncline-central baffle layer.
ABSTRACT
OBJECTIVES: The accuracy of robotic surgery has been recognized by many doctors, but traditional robotic surgery requires 4-5 puncture holes in the operating area. With the popularization and application of single port laparoscopic surgery, the aesthetic of abdominal incision of robotic surgery has been challenged. How to use the single-site platform to complete robot operation is a new field worthy of our exploration. Here we introduce a kind of technology innovation of robot-assisted single-site laparoscopic surgery through common robotic equipment and LAGIS single-site port. METHODS: From November 2018 to March 2019, 20 patients with cervical cancer or endometrial cancer admitted to the minimally invasive gynecological group were included. Single-hole robotic surgery was successfully performed in all 20 patients, with no additional assisted puncture and no conversion to laparotomy. The operation time of patients, intraoperative bleeding volume and hospitalization time were recorded and compared. Besides, the Intraoperative complications were observed and analyzed. RESULTS AND CONCLUSIONS: By comparison, we can find that the effect of this innovative single-hole robotic surgery is significantly better than that of traditional single-hole laparoscopy.
Subject(s)
Laparoscopy , Robotic Surgical Procedures , Robotics , Esthetics , Female , Gynecologic Surgical Procedures , Humans , Robotic Surgical Procedures/adverse effectsABSTRACT
Ovarian cancer is a lethal gynaecologic malignancy with poor diagnosis and prognosis. The long non-coding RNA plasmacytoma variant translocation1 (PVT1) and argonaute 1 (AGO1) are associated with carcinogenesis and chemoresistance; however, the relationship between PVT1 and AGO1 and the downstream mechanisms in ovarian cancer remains poorly known. PVT1 and AGO1 expression was assessed through RT-qPCR and Western blotting in both human tissues and cell lines. The viability and proliferation of ovarian cancer cells were determined by CCK-8 assay and TUNEL assay in vitro and immunohistochemistry in vivo. Cell invasion and migration were investigated through transwell and wound-healing assays. The roles and mechanisms of AGO1 on cell functions were further probed via gain- and loss-of-function analysis. We reveal that PVT1 expression was significantly increased in ovarian cancer tissues which is associated with advanced FIGO stage, lymph-node metastasis, poor survival rate, and high expression of AGO1. PVT1 or AGO1 knockdown significantly reduced the cell viability and increased the cell apoptosis and inhibited ovarian tumour growth and proliferation. Furthermore, we discovered that PVT1 up-regulated the expression of AGO1 and thus regulated the transforming growth factor-ß (TGF-ß) pathway to promote ovarian cancer progression through sponging miR-148a-3p. Additionally, the activation of ERK1/2, smad2 and smad4 is observed to be related to the PVT1/miR-148a-3p/AGO1/TGF-ß pathway-induced cascades. Taken together, the present study reveals that PVT1/miR-148a/AGO1 axis plays an important role in the progression of ovarian cancer and emphasize the potential as a target of value for ovarian cancer therapy.
Subject(s)
Argonaute Proteins/metabolism , Eukaryotic Initiation Factors/metabolism , MicroRNAs/physiology , Ovarian Neoplasms/metabolism , RNA, Long Noncoding/physiology , Animals , Cell Line, Tumor , Cell Proliferation , Female , Gene Expression Regulation, Neoplastic , Humans , Mice, Inbred BALB C , Mice, Nude , Transforming Growth Factor beta/metabolismABSTRACT
In the past decade, several discoveries have documented the existence of innervation in ovarian cancer and cervical cancer. Notably, various neurotransmitters released by the activation of the sympathetic nervous system can promote the proliferation and metastasis of tumor cells and regulate immune cells in the tumor microenvironment. Therefore, a better understanding of the mechanisms involving neurotransmitters in the occurrence and development of gynecological cancers will be beneficial for exploring the feasibility of using inexpensive ß-blockers and dopamine agonists in the clinical treatment of gynecological cancers. Additionally, this article provides some new insights into targeting tumor innervation and neurotransmitters in the tumor microenvironment.
ABSTRACT
Cervical cancer is considered one of the diseases with the highest mortality among women and with limited treatment options. Hydrogen (H2) inhalation has been reported to have a variety of tumorsuppressive effects, but the exact mechanism remains unclear. In the present study, HeLa cervical cancer cells and HaCaT keratinocytes treated with H2, and a HeLa xenograft mouse model subjected to H2 inhalation were established. TUNEL, Cell Counting Kit8 and Ki67 staining assays were used to detect cell apoptosis and proliferation. Oxidative stress was determined according to the levels of reactive oxygen species, malondialdehyde and superoxide dismutase. Tumor growth was recorded every 3 days, and the excised tumors were stained with hematoxylin and eosin. Highthroughput RNA sequencing and subsequent Gene Ontology (GO) enrichment analysis were performed in HeLatreated and untreated HeLa cells. The expression of hypoxiainducible factor (HIF)1α and NFκB p65 was verified by western blotting, immunohistochemistry and reverse transcriptionquantitative PCR. The results revealed an increased apoptosis rate, and reduced cell proliferation and oxidative stress in H2treated HeLa cells but not in HaCaT cells. Similarly, decreased tumor growth and cell proliferation, and enhanced cell apoptosis were observed in H2treated HeLa tumors. RNA sequencing and GO analysis suggest that downregulated HIF1A (HIF1α mRNA) and RelA (NFκB p65) levels, and reduced NFκB signaling were associated with the antitumor effect of H2. Finally, decreased HIF1α and NFκB p65 expression both at the transcriptional and translational levels were observed in H2treated HeLa cells and in HeLaderived tumors. In conclusion, the present study reveals a novel mechanism of H2 against cervical cancer, which may serve as a potential therapeutic target in clinical practice.
Subject(s)
Antineoplastic Agents/administration & dosage , Gene Expression Profiling/methods , Hydrogen/administration & dosage , Hypoxia-Inducible Factor 1, alpha Subunit/genetics , Transcription Factor RelA/genetics , Uterine Cervical Neoplasms/drug therapy , Animals , Antineoplastic Agents/pharmacology , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , Female , Gene Expression Regulation, Neoplastic/drug effects , HeLa Cells , High-Throughput Nucleotide Sequencing , Humans , Hydrogen/pharmacology , Mice , Reactive Oxygen Species/metabolism , Sequence Analysis, RNA , Treatment Outcome , Uterine Cervical Neoplasms/genetics , Uterine Cervical Neoplasms/metabolism , Xenograft Model Antitumor AssaysABSTRACT
PURPOSE: To compare perioperative outcomes between robotic single-site surgical technique and conventional laparoendoscopic single-site surgical technique. METHODS: This was a retrospective cohort study involving 67 patients who received robotic single-site surgery or laparoendoscopic single-site surgery for the treatment of stage IB1 cervical squamous carcinoma. The robotic single-site radical hysterectomy technique combined with pelvic lymph node dissections were performed in 32 patients while the laparoendoscopic single-site radical hysterectomy technique combined with pelvic lymph node dissections were performed in 35 patients. RESULTS: The enrolled patients had been diagnosed with stage IB1 cervical squamous carcinoma. The perioperative outcomes were mean age (51.63±8.32 years in the lymph node dissection (RSS group) and 53.14±8.14 years in the lymph node dissection (LESS group), p=0.453); BMIs (23.76±2.72 in the RSS group and 23.46±2.28 in the LESS group, p=0.629); shorter operative times (223.56±15.43 min in the RSS group and 248.61±20.89 min in the LESS group, p<0.01) and less estimated blood loss (217.25±16.77 mL in the RSS group and 294.74±24.00 mL in the LESS group, p<0.01). None of the study participants exhibited postoperative pain. There were no statistically significant differences in the length of hospital stay (p=0.865), perioperative complications (p=0.602), duration of closure and removal of catheter (p=0.518) as well as in pathological diagnoses between the two groups. CONCLUSION: Robotic single-site surgery can be used in the treatment of early stage cervical cancer as it exhibits acceptable operative times and perioperative outcomes. This surgical technique is feasible and safe.
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Antimetastatic effect of Metformin has been documented in epithelial ovarian cancer (EOC). Presently, we investigated the regulatory mechanism of Metformin in EOC metastasis. First, Girdin was significantly enhanced in EOC tumorous tissues and cell lines. Seconded, knockdown of Girdin significantly suppressed EOC cell viability, migration, and invasion, while upregulation of Girdin produced the opposite effects in vitro and facilitated lung metastasis in EOC cell xenograft in vivo. In addition, we confirmed that the inhibitory effect of Metformin on Girdin expression. Mechanistically, the oncogenic effects of Girdin could be reversed by LY294002 (an AKT pathway inhibitor) and Metformin. These results suggested that Metformin attenuated EOC metastasis through Girdin and targeting Girdin may be a promising therapeutic strategy for EOC in the future.
Subject(s)
Carcinoma, Ovarian Epithelial/metabolism , Microfilament Proteins/genetics , Neoplasm Metastasis/drug therapy , Vesicular Transport Proteins/genetics , Adult , Animals , Carcinoma, Ovarian Epithelial/genetics , Carcinoma, Ovarian Epithelial/pathology , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Cell Survival/genetics , Epithelial-Mesenchymal Transition , Female , Gene Expression/genetics , Gene Expression Profiling/methods , Gene Expression Regulation, Neoplastic/genetics , Humans , Metformin/metabolism , Metformin/pharmacology , Mice, Nude , Microfilament Proteins/drug effects , Microfilament Proteins/metabolism , Middle Aged , Neoplasm Invasiveness/genetics , Neoplasm Metastasis/genetics , Ovarian Neoplasms/genetics , Ovarian Neoplasms/metabolism , Ovarian Neoplasms/pathology , Transcriptome/genetics , Vesicular Transport Proteins/drug effects , Vesicular Transport Proteins/metabolismABSTRACT
Long non-coding RNA (lncRNA) has increasingly been identified as a key regulator in pathologies such as cancer. Multiple platforms were used for comprehensive analysis of ovarian cancer to identify molecular subgroups. However, lncRNA and its role in mapping the ovarian cancer subpopulation are still largely unknown. RNA-sequencing and clinical characteristics of ovarian cancer were acquired from The Cancer Genome Atlas database (TCGA). A total of 52 lncRNAs were identified as aberrant immune lncRNAs specific to ovarian cancer. We redefined two different molecular subtypes, C1(188) and C2(184 samples), in "iClusterPlus" R package, among which C2 grouped ovarian cancer samples have higher survival probability and longer median survival time (P <0.05) with activated IFN-gamma response, Wound Healing and Cytotoxic lymphocytes signal; 456 differentially expressed genes were acquired in C1 and C2 subtypes using limma (3.40.6) package, among which 419 were up-regulated and 37 were down-regulated, in TCGA dataset. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis revealed that these genes were actively involved in ECM-receptor interaction, PI3K-Akt signaling pathway interaction KEGG pathway. Compared with the existing immune subtype, the Cluster2 sample showed a substantial increase in the proportion of the existing C2 immune subtype, accounting for 81.37%, which was associated with good prognosis. Our C1 subtype contains only 56.49% of the existing immune C1 and C4, which also explains the poor prognosis of C1. Furthermore, 52 immune-related lncRNAs were used to divide the TCGA-endometrial cancer and cervical cancer samples into two categories, and C2 had a good prognosis. The differentially expressed genes were highly correlated with immune-cell-related pathways. Based on lncRNA, two molecular subtypes of ovarian cancer were identified and had significant prognostic differences and immunological characteristics.
Subject(s)
Gene Expression Regulation, Neoplastic , Ovarian Neoplasms/genetics , Ovarian Neoplasms/immunology , RNA, Long Noncoding/genetics , Endometrial Neoplasms/genetics , Endometrial Neoplasms/immunology , Endometrial Neoplasms/pathology , Female , Gene Expression Profiling , Humans , Ovarian Neoplasms/pathology , RNA, Long Noncoding/metabolism , Uterine Cervical Neoplasms/genetics , Uterine Cervical Neoplasms/immunologyABSTRACT
Thermochemical sulfate reduction (TSR) is common in marine carbonate gas reservoirs, leading to complicated isotope characteristics of TSR-altered gas. This study aims to better understand how TSR affects the geochemical and isotopic compositions of alkanes in pyrolysis products. Pyrolysis of TSR were conducted with crude oil, nonane (C9) and methylnaphthalene (MN) in the presence of MgSO4 solution at temperatures of 350 °C, 360 °C, and 370 °C for different durations of 4-219 h in a closed system. Results show that carbon and hydrogen isotope compositions of alkane gas resulting from TSR (pyrolysis with crude oil and MgSO4) became heavier with increasing carbon number, i.e., δ13C1 < δ13C2 < δ13C3 and δ2H-C1 < δ2H-C2 < δ2H-C3. Compared with the δ13C1, δ13C2 and δ13C3 increased in a much wider range as heating continued. Carbon and hydrogen isotopes of alkane gas produced by TSR became heavier with increasing gas souring index. Values for δ13C1-δ13C2 and δ2H-C1- δ2H-C2 typically decreased as oil and C9 underwent thermal cracking. Comparative experiments using C9 in the presence of MgSO4 produced partially reversed carbon isotope series (δ13C1 > δ13C2), which, for the first time, confirmed the ability of TSR to cause isotopic reversal from pyrolysis. The residual heavy alkanes gradually became 13C-enriched during TSR, which increased δ13C2 values and changed the partially reversed isotope sequence to a positive sequence (δ13C1 < δ13C2). The discovery of a partial reversal of the carbon isotope series of alkane gases through pyrolysis will further deepen the understanding of TSR-altered natural gas.
ABSTRACT
BACKGROUND: Ovarian cancer is one of the most common gynecologic cancers with high morbidity and mortality in women. Glycogen metabolism plays a critical role in cancer development and glycogen phosphorylase B (PYGB) has reported to be involved in various tumors. Here, we explored the role of PYGB in ovarian cancer. METHODS: PYGB mRNA expression were examined in ovarian cancer tissue and also analyzed using the dataset from The Cancer Genome Atlas cohort. Correlations between PYGB expression and prognosis of ovarian cancer patients were analyzed. PYGB was silenced to evaluate the ovarian cell proliferation, invasion and migration in vitro and tumorigenesis in vivo. MiR-133a-3p targeting PYGB was identified using online tools and confirmed with luciferase reporter experiment. MiR-133a-3p overexpression using miRNA mimics was conducted to evaluate its function on ovarian cancer cells. RESULTS: We showed that PYGB was upregulated in ovarian cancer tissue and high level of PYGB expression is markedly correlated with poor prognosis of ovarian cancer patients. PYGB knockdown significantly suppressed ovarian cancer cell proliferation, invasion and migration. Xenograft tumor formation further demonstrated that knockdown PYGB inhibited ovarian tumor development. Bioinformatics analysis revealed that PYGB regulated Wnt/ß-catenin signaling pathway in ovarian cancer cells. Mechanistically, miR-133a-3p directly bound to 3'-untranslated region of PYGB and overexpression miR-133a-3p suppressed proliferation, invasion and migration in ovarian cancer cells. CONCLUSION: Our data suggest that miR-133a-3p/PYGB/Wnt-ß-catenin axis plays a critical role in human ovarian cancer, which might serve as a promising therapeutic target of ovarian cancer treatment in the future.
Subject(s)
Glycogen Phosphorylase, Brain Form/metabolism , MicroRNAs/metabolism , Ovarian Neoplasms/metabolism , Wnt Signaling Pathway , beta Catenin/metabolism , Animals , Cell Line, Tumor , Cell Movement/physiology , Cell Proliferation/physiology , Disease Progression , Female , Glycogen Phosphorylase, Brain Form/biosynthesis , Glycogen Phosphorylase, Brain Form/genetics , HEK293 Cells , Heterografts , Humans , Male , Mice , Mice, Inbred BALB C , Mice, Nude , MicroRNAs/genetics , Ovarian Neoplasms/genetics , Ovarian Neoplasms/pathology , Prognosis , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Up-RegulationABSTRACT
OBJECTIVE: (1) to investigate the expression of long non-coding RNA (lncRNA) H19 in OVCAR3 and cisplatin-resistant OVCAR3/DDP cells; (2) to explore the effects of lncRNA H19 on cisplatin-resistance in ovarian cancer (OC) cells; (3) to determine the roles of lncRNA H19 on OC cell migration and epithelial to mesenchymal transition (EMT)-related factors. METHODS: The human ovarian cancer OVCAR3 cell line was obtained from ATCC; the cisplatin-resistant OVCAR3/DDP cell line was induced from OVCAR3 cells through a progressive cisplatin concentration; OVCAR3 cells that overexpress lncRNA H19 and OVCAR3/DDP cells that silence the lncRNA H19 expression were established by the transfection of a recombinant lentivirus. A cell counting kit-8 (CCK-8) assay was used to determine the cell viability of OVCAR3 and OVCAR3/DDP. A reverse transcription-quantitative polymerase chain reaction (RT-qPCR) demonstrated the expressions of lncRNA H19, E-cadherin, twist, slug, and snail mRNA in OVCAR3 and OVCAR3/DDP cells. A Transwell assay was used to investigate the migration of OVCAR3 and OVCAR3/DDP cells. The expressions of E-cadherin, twist, slug, and snail proteins were determined by Western blot. RESULTS: The cisplatin-resistant OVCAR3/DPP cells were successfully established. The level of lncRNA H19 in the OVCAR3/DDP cells was significantly elevated compared with the OVCAR3 cells (P < 0.05). The overexpression of lncRNA in the OVCAR3 cells improved the cisplatin-resistance, and the inhibition of lncRNA H19 expression in OVCAR3/DDP cells eliminated the cisplatin resistance. Furthermore, the migration ability and the expressions of the EMT positive regulator, twist, slug, snail mRNA, and protein in OVCAR3/DDP were dramatically up-regulated compared with the OVCAR3 group, and the expressions of the EMT negative regulator, E-cadherin mRNA, and protein were decreased compared with the OVCAR3 group, suggesting an increase of migration and EMT ability was observed in the OVCAR3/DDP cells. A gain of lncRNA expression in the OVCAR3 cells promoted migration and EMT-related activity; the loss of lncRNA H19 expression eliminated the enhanced ability of migration and EMT in the OVCAR3/DDP cells. CONCLUSIONS: LncRNA H19 is responsible for the cisplatin-resistance, migration, and MET regulation in OVCAR3 cells.
ABSTRACT
A consensus has been reached through previous studies that organic matter (OM) pores are crucial to porosity in many shale gas reservoirs; however, their origins and types remain controversial. Here, we report the OM pore types hosted in algae, bitumen, graptolite and other fossil fragments in the Wufeng-Longmaxi Formations of the Sichuan Basin, Southwest China. Algae types mainly include multicellular algae, unicellular algae, etc. The OM pores in multicellular algae usually exhibit irregular, bubble-like, spherical and/or elliptical profiles, and their diameters vary between 300 and 800 nm. The shapes of the OM pores in unicellular algae are either irregular or oval, and the pores are hundreds of nanometres in size. The pores associated with solid bitumen are sporadic, isolated and variable in size, ranging from 500 nm to 3 µm. The pores in the graptolite, sponge spicule, radiolarian and other fossil fragments are much smaller and fewer. The pores may only have developed in the surface of the graptolite and bitumen by filling in the biological cavity of the sponge spicule. These new findings provide stronger evidence that multicellular algae are the main hydrocarbon generating organisms of OM pores development.
Subject(s)
Fossils/ultrastructure , Hydrocarbons/analysis , China , Hydrocarbons/chemistry , Microalgae/chemistryABSTRACT
OBJECTIVE: Specific sgRNA-sequences targeting oncogenes E6 and E7 in HPV18 were designed using the CRISPR/Cas9 system. These sgRNAs knocked out E6 and E7 expressions and were used to study their effects on the proliferation and cell cycle of the cervical cancer HeLa cell line. METHODS: Lentivirus vectors targeting E6 and E7 oncogenes were constructed and transfected into HeLa cells. mRNA and protein expression levels of E6 and E7 were measured by RT-PCR and Western blot, respectively. The cell cycle was detected by flow cytometry. A colony formation assay was applied to evaluate the proliferation capacity of the HeLa cells. RESULTS: Three E6 Cas9-sgRNA vectors targeting E6 and three E7 Cas9-sgRNA vectors targeting E7 genes were constructed and transfected into HeLa cells, respectively. RT-PCR results showed that all three E6 and E7 sgRNAs inhibited the expressions of E6 or E7 mRNA, respectively, when compared with the control groups. The inhibition ratios of the three groups of E6-sgRNAs were 28%, 85%, and 19%; the E7-sgRNAs were 86%, 25%, and 27%, respectively (P<0.05), with E6-sgRNA2 and E7-sgRNA1 having the greatest inhibitory effects. Western blot results showed that, compared with the control group, the protein expressions of E6 and E7 in the sgRNAs transfected group were also decreased, and E6-sgRNA2 and E7-sgRNA1 had the most inhibitory effects on E6 and E7 proteins. Flow cytometry results showed that the number of cells in G1/G0 was increased by 14.2% in the E6-sgRNA2 transfection group, and by 7.1% in the E7-sgRNA1 transfection group. Colony formation assay results showed that after transfection of E6 or E7 sgRNA plasmids, the HeLa cell colony was reduced significantly compared with the control group. CONCLUSIONS: The CRISPR/Cas9 system targeting HPV18 E6 or E7 genes effectively blocked the transcription and expression of oncogenes E6 or E7 in HeLa cells, which resulted in cell cycle arrest and reduced cell proliferation.