1-Monopalmitin promotes lung cancer cells apoptosis through PI3K/Akt pathway in vitro.

Lung cancer is the leading cause of cancer-related death worldwide and non-small cell lung cancer (NSCLC) represents 85%. Mougeotia nummuloides and Spirulina major have been reported to possess anticancer properties. 1-Monopalmitin (1-Mono) is the principle active constituent in these natural plants. It is debating whether 1-Mono exerts antitumor effects. Therefore, we explored the role of 1-Mono in lung cancer in vitro. Results showed that 1-Mono significantly inhibited A549 and SPC-A1 cell proliferation, induced G2/M arrest and caspase-dependent apoptosis. Moreover, it suppressed the protein expression of inhibitors of apoptosis proteins (IAPs). It was further demonstrated that 1-Mono activated the PI3K/Akt pathway, suppression of PI3K/Akt activities with LY294002 and Wortmannin partially attenuated 1-Mono-mediated anticancer activities, indicating that 1-Mono-induced antitumor effects is dependent on PI3K/Akt pathway. 1-Mono induced cytoprotective autophagy since autophagy inhibitor Chloroquine dramatically enhanced 1-Mono-induced cytotoxicity. In summary, our results showed 1-Mono kills lung cancer through PI3K/Akt pathway, providing novel options for lung cancer administration.

Brexpiprazole suppresses cell proliferation and de novo lipogenesis through AMPK/SREBP1 pathway in colorectal cancer.

OBJECTIVE: In the present study, we investigated the role of brexpiprazole on cell proliferation and lipogenesis in colorectal cancer (CRC) and its molecular mechanism. METHODS: The effect of brexpiprazole on CRC cell proliferation was determined by CCK-8, EdU assay, cell clone formation. The flow cytometry was evaluated cell cycle. Differential expression genes (DEGs) were identified by RNA-seq assay after treating HCT116 cells with or without 20 µM brexpiprazole for 24 h. Then, the top 120 DEGs were analyzed by GO and KEGG enrichment analysis. After that, Oil red O staining and the levels of total cholestenone and triglyceride were measured to assess lipogenesis capacity in CRC cells. The related molecules of cell proliferation, lipogenic and AMPK/SREBP1 signal pathways were measured by q-PCR, western blot and immunohistochemical staining. RESULTS: Brexpiprazole remarkably suppressed cell proliferation, lipogenesis, and induced cell cycle arrest in CRC. The underlying mechanisms probably involved the suppression of SREBP1 and the stimulation of AMPK. CONCLUSION: Brexpiprazole inhibited cell proliferation and de novo lipogenesis through AMPK/SREBP1 pathway in CRC.

Trends in the evolution of sustainable development research in China: a scientometric review.

Because of the extensive attention of global scholars on the sustainable development in China, much research has been published over the past 30 years. Based on the 12,635 journal papers from the Web of Science database, we explore the trends in the evolution of China's sustainable development research by a knowledge graph. The result indicates that the attention of China's sustainable development research increased exponentially during 1991-2021, and it continues to shift from a macroperspective to the exploration of specific methods and implementation paths. During 2001-2005, China's sustainable development research developed rapidly and formed a complete cluster structure. In addition, China's sustainable development research has experienced three stages and two topic drifts. Staged development and topic drifts lead to a wide range of disciplinary drifts. In general, the trends in the evolution of China's sustainable development research mainly focus on three aspects: research methods, research scope, and theoretical innovation. China's sustainable development provides a case or a path for other developing countries. Economic incentives and policy promotion remain important measures to promote sustainable development.

The role of NEDD4 related HECT-type E3 ubiquitin ligases in defective autophagy in cancer cells: molecular mechanisms and therapeutic perspectives.

The homologous to the E6-AP carboxyl terminus (HECT)-type E3 ubiquitin ligases are the selective executers in the protein ubiquitination, playing a vital role in modulation of the protein function and stability. Evidence shows the regulatory role of HECT-type E3 ligases in various steps of the autophagic process. Autophagy is an intracellular digestive and recycling process that controls the cellular hemostasis. Defective autophagy is involved in tumorigenesis and has been detected in various types of cancer cells. A growing body of findings indicates that HECT-type E3 ligases, in particular members of the neural precursor cell expressed developmentally downregulated protein 4 (NEDD4) including NEDD4-1, NEDD4-L, SMURFs, WWPs, and ITCH, play critical roles in dysregulation or dysfunction of autophagy in cancer cells. The present review focuses on NEDD4 E3 ligases involved in defective autophagy in cancer cells and discusses their autophagic function in different cancer cells as well as substrates and the signaling pathways in which they participate, conferring a basis for the cancer treatment through the modulating of these E3 ligases.

miR-223-3p mediates the diabetic kidney disease progression by targeting IL6ST/STAT3 pathway.

Diabetic kidney disease (DKD), the most pervasive complication in diabetic patients, has become a major health threat to the aging population. Our previous miRNA profiling identified hsa-miR-223-3p as a dysregulated miRNA in the DKD samples, which may serve as a biomarker for DKD diagnosis. However, the specific mechanism of miR-223-3p in the pathogenesis of DKD remains to be elucidated. In this study, we first verified that miR-223-3p level was significantly decreased in the in vitro cell model and in vivo db/db DKD model, accompanied with endothelial cell damage. Importantly, inhibiting the expression of miR-223-3p exacerbated high-glucose induced damages in Human Umbilical Vein Endothelial Cells (HUVECs) and Human Renal Glomerular Endothelial Cells (HRGECs), while miR-223-3p overexpression showed the opposite effect. We further demonstrated that miR-223-3p associated with IL6T mRNA and attenuated the progression of DKD by suppressing the downstream STAT3 activation, indicative of the implication of miR-223-3p/IL6T/STAT3 axis in the pathogenesis of DKD.

Maintenance of the Expression of c-FLIPL by Hsp70 to Resist Licochalcone A-Induced Anti-Colorectal Cancer Effect through ERK-Mediated Autophagy Induction.

BACKGROUND: The mortality rate of colorectal cancer (CRC) ranks second worldwide. Previous research had indicated that licochalcone A (LA) was a flavonoid in licorice with diverse anticancer effects. We explored the underlying mechanisms of LA-triggered anticancer activity in CRC. METHODS: Thiazolyl Blue (MTT) experiment and EdU staining were utilized to evaluate cell proliferation. Meanwhile, cells were stained by Annexin V/PI to investigate apoptosis through flow cytometry assay. Moreover, expressions of proteins were detected by immunoblotting, and the level of related mRNA was investigated using real-time quantitative PCR. RESULTS: LA selectively suppressed the proliferation and triggered apoptosis of CRC cells. Strikingly, LA induced cytoprotective autophagic activities since the suppression of autophagy significantly strengthened LA-induced cytotoxicity and FLICE inhibitory protein (c-FLIPL) degradation, meanwhile reversing LA-mediated heat shock protein 70 (Hsp70) upregulation. Moreover, autophagy-mediated Hsp70 upregulation resisted LA-induced anticancer effects since the suppression of Hsp70 strengthened LA-triggered cytotoxicity and c-FLIPL degradation. Furthermore, LA greatly activated extracellular signal-regulated protein kinases (ERK) and p38. However, blocking of ERK, but not p38, significantly boosted LA-triggered cell death and c-FLIPL downregulation. Suppression of ERK also reversed LA-mediated autophagic induction. CONCLUSIONS: LA increased Hsp70 expression depending on ERK-mediated autophagy, which protected CRC cells from LA-induced anticancer activities.

Stem cell-derived and circulating exosomal microRNAs as new potential tools for diabetic nephropathy management.

BACKGROUND: Despite major advances in the treatment of diabetic nephropathy (DN) in recent years, it remains the most common cause of end-stage renal disease. An early diagnosis and therapy may slow down the DN progression. Numerous potential biomarkers are currently being researched. Circulating levels of the kidney-released exosomes and biological molecules, which reflect the DN pathology including glomerular and tubular dysfunction as well as mesangial expansion and fibrosis, have shown the potential for predicting the occurrence and progression of DN. Moreover, many experimental therapies are currently being investigated, including stem cell therapy and medications targeting inflammatory, oxidant, or pro-fibrotic pathways activated during the DN progression. The therapeutic potential of stem cells is partly depending on their secretory capacity, particularly exosomal microRNAs (Exo-miRs). In recent years, a growing line of research has shown the participation of Exo-miRs in the pathophysiological processes of DN, which may provide effective therapeutic and biomarker tools for DN treatment. METHODS: A systematic literature search was performed in MEDLINE, Scopus, and Google Scholar to collect published findings regarding therapeutic stem cell-derived Exo-miRs for DN treatment as well as circulating Exo-miRs as potential DN-associated biomarkers. FINDINGS: Glomerular mesangial cells and podocytes are the most important culprits in the pathogenesis of DN and, thus, can be considered valuable therapeutic targets. Preclinical investigations have shown that stem cell-derived exosomes can exert beneficial effects in DN by transferring renoprotective miRs to the injured mesangial cells and podocytes. Of note, renoprotective Exo-miR-125a secreted by adipose-derived mesenchymal stem cells can improve the injured mesangial cells, while renoprotective Exo-miRs secreted by adipose-derived stem cells (Exo-miR-486 and Exo-miR-215-5p), human urine-derived stem cells (Exo-miR-16-5p), and bone marrow-derived mesenchymal stem cells (Exo-miR-let-7a) can improve the injured podocytes. On the other hand, clinical investigations have indicated that circulating Exo-miRs isolated from urine or serum hold great potential as promising biomarkers in DN.

Boeravinone B alleviates gut dysbiosis during myocardial infarction-induced cardiotoxicity in rats.

Myocardial infarction (MI) is the most common heart disease, and also, it is one of the leading causes of death from cardiovascular disease. It is well known that MI causes additional injury during blood flow restoration in ischaemic myocardium. Boeravinone B (BB) is a well-known antioxidant and anti-inflammatory drug. We investigated the cardioprotective effect of BB drug against isoproterenol (ISO)-induced MI in rats in this experimental study, along with we analysed its underlying mechanism. Adult Sprague Dawley (SD) rats were treated subcutaneously with ISO (45 mg/kg), then divided into groups and then given BB drug was administered orally. The cardioprotective effect of BB on ISO-induced MI rats was analysed by estimating the heart injury markers, antioxidant pro-inflammatory cytokines and inflammatory parameters. We also detected quantified expression of inflammation and apoptosis-related marker protein family. We estimated the effect of BB drug on GUT microbiota in ISO-induced MI rats and scrutinized the histopathological variations in heart tissues. BB treatment significantly (P < .001) diminished the level of heart markers such as lactate dehydrogenase (LDH), troponin (TnT), creatine kinase (CK) and creatine kinase isoenzymes MB (CK-MB). BB treatment also altered the antioxidant parameters and reduced the pro-inflammatory cytokines in the serum and tissues. Additionally, the histopathological aspects demonstrated that the pathological changes observed in the heart tissue of the ISO group rats were suppressed by the BB treatment to varying degrees. Furthermore, the expressions of caspase-3, p53, caspase-9, Bax, interleukin-6 (IL-6), cytochrome C, neutrophil gelatinase-associated lipocalin (NGAL), tumour necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB) and interleukin-1ß (IL-1ß) in the heart tissue were down-regulated whereas the Bcl-2 expression seemed to be enhanced. BB treatment not only alleviated ISO-induced gut dysbiosis by its enhanced specified Firmicutesto-Bacteroidetes (F/B) ratio but also maintained the relative abundance of major bacteria such as Clostridium IV, Butyricicoccus, Clostridium XIVs, Akkermansia and Roseburia. Collectively, our findings showed that the BB drug acted against myocardial infraction and prevented the damage by reducing the oxidative stress and controlling the inflammatory pathways, and gut microbiota.

Tunable Electrocatalytic Annulations of o-Arylalkynylanilines: Green and Switchable Syntheses of Skeletally Diverse Indoles.

Tunable electrocatalytic annulation reactions of o-arylalkynylanilines have been established, leading to green and divergent syntheses of skeletally diverse indoles by adjusting the electrolytes and the solvents. The presence of ammonium halides as the electrolytes enabled the halogenation of o-arylalkynylanilines to give C3-halogenated indoles whereas naphtho[1',2':4,5]furo[3,2-b]indoles could be obtained by changing the electrolyte from ammonium halides to KI. Interestingly, by combining acetone as the solvent and both NH4I and NH4Cl as the electrolytes, the reaction worked through an intramolecular annulation and [5 + 1] cyclization cascade to form naphtho[1',2':5,6][1,3]oxazino[3,4-a]indoles.

Evaluation of cervical maturity by cervical collagen measurement using light-induced fluorescence (LIF) during pregnancy.

OBJECTIVE: The study aimed to evaluate cervical ripening by measuring cervical collagen levels in non-pregnant women, women with a normal pregnancy, and postpartum women by light-induced fluorescence (LIF). METHODS: Cervical collagen content in normal pregnant women (n = 165) at various times of gestation was measured by LIF with a collascope, which is specifically designed to measure fluorescence of collagen. Cervical LIF in non-pregnant women (n = 12) and postpartum women (n = 14) was also detected. The demographic characteristics of women at various times were recorded. The Bishop score at 40 to 41 gestational weeks (n = 37) before the onset of labor was analyzed. RESULTS: Cervical LIF values progressively declined from the non-pregnant state to late gestation (R = -0.836) and reached their lowest levels during parturition and then increased at postpartum. LIF values and the Bishop score were significantly negatively correlated (R = -0.83). In patients with a Bishop score ≥6, the first stage of labor was shortened with a decrease in LIF values (R = 0.718). CONCLUSIONS: Cervical collagen levels as measured by LIF could be a useful method for evaluating cervical maturity.

ERK Activation-Mediated Autophagy Induction Resists Licochalcone A-Induced Anticancer Activities in Lung Cancer Cells in vitro.

INTRODUCTION: The incidence and mortality rates of lung cancer rank top in the different types of cancers in China. Licochalcone A (LA) is a flavonoid extracted from the roots of licorice with antitumor effects in various cancers in vitro and in vivo. However, the role of LA in non-small cell lung cancer (NSCLC) remains largely unclear. METHODS: The cell viability was measured by MTT assay, Edu staining and colony formation assay. Apoptosis was investigated using Annexin V/PI double-stained assays with flow cytometry. Real-time quantitative RT-PCR was carried out to investigate the expression of mRNA of related proteins. Western blotting was used to investigate the expression of related proteins. RESULTS: The results show that LA inhibits the proliferation of NSCLC cells in a dose-dependent manner and induces apoptotic cell death. Moreover, LA significantly suppresses the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL and RIP1 without influencing the level of mRNA. Cycloheximide chase assay demonstrates that LA greatly decreases the stability of Survivin, XIAP and RIP1. Mechanistic studies indicate that LA induces cytoprotective autophagy since block of autophagy with CQ greatly enhances LA-induced anticancer activities. Furthermore, LA rapidly induces ERK and p38 activation in a time-dependent manner in both A549 and H460 cells, but suppresses the activities of c-Jun N-terminal kinase (JNK); suppression of ERK not p38 with inhibitor attenuates LA-induced autophagy, while it remarkably enhances LA-induced cytotoxicity in lung cancer cells and further promotes the degradation of apoptosis-related proteins. DISCUSSION: The results of this study provide novel insights on the role of apoptosis-related proteins and the MAPKs pathway in the anticancer activities of LA.

Gold nano particles synthesized from Magnolia officinalis and anticancer activity in A549 lung cancer cells.

Nanotechnology is creating a bang in each and every field of life science. Scientists are mounting their interest of research towards gold nanoparticles as they are capable with bigger and advanced properties.Traditionally nanoparticles have been manufactured by various chemical and physical methods but have negative impact on the environment and are also highly toxic. Synthesis of nanoparticles by using plant extracts is substituting the conventional methods and it is eco-friendly too. In the current study, we prepared gold nanoparticles (AuNPs) from Magnolia officinalis, which is identified as an eco-friendly and less toxic method. Incorporation of AuNPs was renowned by UV-absorbance and it shows peak values. Nanoparticle sizes are recognized by dynamic light scattering scrutiny and it shows a value of 128 nm. Besides, high resolution transmission electron microscopy (HR-TEM), energy dispersive X-ray analysis (EDX) and atomic force microscopy (AFM) incorrigibly define the shape of the AuNPs which are present in the complex materials. Fourier-transform infrared spectroscopy (FTIR) findings display that the active molecules are positioned in the plane of the AuNPs. Similarly, anticancer efficacy of AuNPs have been assessed in A549 cells. our study show that AuNPs effectively provoke cytotoxicity, and apoptosis by inflecting apoptotic gene expressions in A549 cells.

Measurement of Uterine and Abdominal Muscle Electromyography in Pregnant Women for Estimation of Expulsive Activities during the 2nd Stage of Labor.

BACKGROUND: The progression of labor and delivery of the fetus is dependent upon uterine contractions and the voluntary effort of abdominal muscle contractions. A good monitor of uterine contractions and pushing is necessary for obstetrical care. Electromyography (EMG) is the underlying basis for contractility of muscle including the myometrium. OBJECTIVES: The aim of this study was to determine the relationship between EMG activity of uterine and abdominal muscles and the duration of the 2nd stage of labor in pregnant women. METHODS: EMG of both uterine and abdominal muscles was simultaneously recorded from electrodes placed on the abdominal surface of 45 active 2nd stage-laboring nulliparous patients. EMG was recorded using filters to separate uterine and abdominal EMG signals, and various EMG signal parameters were analyzed. The duration of the 2nd stage of labor and other maternal and fetal characteristics were also recorded. RESULTS: Uterine EMG bursts precede abdominal bursts and are accompanied by feelings of "urge to push" by the patients. Abdominal root mean square (RMS) and power, but not uterine EMG parameters, are reduced (p< 0.005) in patients with longer labors and linear regression analysis demonstrated a negative correlation to the duration of 2nd stage of labor (p < 0.001). Multivariate linear regression analysis of clinical characteristics (fetal weight, body mass index, placental location, etc.) and parameters of EMG showed that only abdominal RMS is negatively correlated with the duration of labor. CONCLUSIONS: (1) Uterine and abdominal EMG activities reflect the expulsive involuntary (uterine) and voluntary (abdominal) muscular activities during the 2nd stage of labor. (2) RMS and power of abdominal EMG diminish with longer labor when uterine EMG intensities are similar. (3) Recording of uterine and abdominal muscle activity provides objective evaluation of the muscle activity during the 2nd stage of labor and may aid in the evaluation of any interventions.

Metformin promotes survivin degradation through AMPK/PKA/GSK-3ß-axis in non-small cell lung cancer.

Metformin, a first-line antidiabetic drug, has been reported with anticancer activities in many types of cancer. However, its molecular mechanisms remain largely unknown. As a member of inhibitor of apoptosis proteins, survivin plays an important role in the regulation of cell death. In the present study, we investigated the role of survivin in metformin-induced anticancer activity in non-small cell lung cancer in vitro. Metformin mainly induced apoptotic cell death in A549 and H460 cell lines. It remarkably suppressed the expression of survivin, decreased the stability of this protein, then promoted its proteasomal degradation. Moreover, metformin greatly suppressed protein kinase A (PKA) activity and induced its downstream glycogen synthase kinase 3ß (GSK-3ß) activation. PKA activators, both 8-Br-cAMP and forskolin, significantly increased the expression of survivin. Consistently both GSK-3ß inhibitor LiCl and siRNA restored the expression of survivin in lung cancer cells. Furthermore, metformin induced adenosine 5'-monophosphate-activated protein kinase (AMPK) activation. Suppression of the activity of AMPK with Compound C reversed the degradation of survivin induced by metformin, and meanwhile, restored the activity of PKA and GSK-3ß. These results suggest that metformin kills lung cancer cells through AMPK/PKA/GSK-3ß-axis-mediated survivin degradation, providing novel insights into the anticancer effects of metformin.

Metformin induces apoptotic cytotoxicity depending on AMPK/PKA/GSK-3ß-mediated c-FLIPL degradation in non-small cell lung cancer.

BACKGROUND: Metformin, a first-line antidiabetic drug, has recently been reported with anticancer activities in various cancers; however, the underlying mechanisms remain elusive. The aim of the present study was to investigate the role of cellular FADD-like IL-1ß-converting enzyme (FLICE)-inhibitory protein large (c-FLIPL) in metformin-induced anticancer activity in non-small cell lung cancer (NSCLC) in vitro. MATERIALS AND METHODS: Cell viability was measured by MTT assay. Quantitative real-time PCR was carried out to detect the level of mRNA of related genes. The expression of related proteins was detected by Western blot. siRNA was used to silence the expression of targeted proteins. RESULTS: Metformin significantly suppressed proliferation of both A549 and H460 cells in a dose-dependent manner. Mechanistic studies suggested that metformin killed NSCLC cells by inducing apoptotic cell death. Moreover, metformin greatly inhibited c-FLIPL expression and then promoted its degradation. Furthermore, metformin significantly activated Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) and its downstream glycogen synthase kinase 3beta (GSK-3ß), block the expression of AMPK, and GSK-3ß with siRNA partially reversed metformin-induced cytotoxicity and restored the expression of c-FLIPL in lung cancer cells. Metformin also suppressed the activity of AMPK downstream protein kinase A (PKA), PKA activators, both 8-Br-cAMP and forskolin, greatly increased c-FLIPL expression in NSCLC cells. CONCLUSION: This study provided evidence that metformin killed NSCLC cells through AMPK/PKA/GSK-3ß axis-mediated c-FLIPL degradation.

WWP2 Is One Promising Novel Oncogene.

WWP2 is an E3 ubiquitin ligase and plays an important role in regulation of many cellular biological activities through ubiquitination and degradation of its substrates. Recently accumulating evidences indicate that WWP2 plays a crucial part in the pathogenesis in different types of tumors. In this report, the role of this gene especially in tumorigenesis was reviewed. WWP2 is dysregulated in various of tumors, and it promotes carcinogenesis mainly through PTEN/Akt signaling pathway. WWP2 also participates in anti-cancer agents' sensitivity, indicating WWP2 may be a novel target for cancer treatment. WWP2 is one promising novel oncogene.

Choline Supplementation During Pregnancy Protects Against Gestational Lipopolysaccharide-Induced Inflammatory Responses.

OBJECTIVES: To estimate the effects and mechanisms of choline, an essential nutrient and a selective α7 nicotinic acetylcholine receptor (α7nAChR) agonist, on the prevention of symptoms and the effects on the cholinergic anti-inflammatory pathways (CAP) in a lipopolysaccharide (LPS)-induced inflammatory response in a rat model. METHODS: Inflammation was induced by LPS treatment (1.0 µg LPS/kg body weight) on gestational day (GD) 14. Nonpregnant and pregnant Sprague Dawley rats were placed on a normal choline diet (1.1 g/kg) or supplemented choline diet (5.0 g/kg) from GDs 1 to 20. Systolic blood pressure (SBP), urinary albumin, and pregnancy outcomes were recorded. On GD 20, serum and placentas were assayed for cytokines. Western blots were used to determine the expression of placenta α7nAChR and components of the α7nAChR-CAP, including nuclear factor-κB (NF-κB) and protein kinase B (AKT). Immunohistochemistry was used to localize placental sites for the p65 subunit of NF-κB. RESULTS: Lipopolysaccharide significantly increased SBP and urinary albumin and decreased pregnancy outcomes, and these effects were partially reversed by higher choline treatment. Choline supplementation also significantly attenuated the LPS-induced increase in serum and placental inflammatory cytokines, decreased the expression of placental α7nAChR, lowered the activation of NF-κB signaling in placenta mononuclear cells, and inhibited placental AKT phosphorylation. CONCLUSION: This study confirms that LPS induces inflammatory conditions in pregnant rats and shows that choline supplementation protects against the inflammatory symptoms through its action on α7nAChR and CAP. These observations have important implications for the prevention and treatment of inflammatory responses associated with pregnancy.

CRTC2 promotes non-small cell lung cancer A549 migration and invasion in vitro.

BACKGROUND: CRTC2 is highly expressed in lung cancer and contributes to lung cancer pathogenesis; however, whether CRTC2 promotes lung cancer metastasis remains unknown. In the present study, we investigated the role of CRTC2 in lung cancer metastasis in vitro. METHODS: CRTC2 stable knockdown of lung cancer cell A549 was generated with small hairpin RNA and confirmed by quantitative reverse transcription-PCR and Western blot. Wound healing and invasion transwell assays were performed to explore migration and invasion activity, and Western blot was conducted to detect the expression of related proteins. RESULTS: Suppression of CRTC2 significantly inhibited A549 cell migration and invasion in vitro. Mechanistic studies showed that knockdown of CRTC2 greatly downregulated MMP2 and MMP9 expression. CRTC2 silencing remarkably suppressed epithelial-mesenchymal transition by modulating the expression of E-cadherin and vimentin. Furthermore, suppression of CRTC2 expression significantly reduced MAPK/c-Jun N-terminal kinase activity. CONCLUSION: CRTC2 may promote A549 migration and invasion by modulation of c-Jun N-terminal kinase-mediated epithelial-mesenchymal transition and matrix metalloproteinase expression.

Primary clear cell carcinoma of the trachea: A CARE-compliant case report.

RATIONALE: Primary clear cell carcinoma of the lung is a rare condition, and presentation as an endotracheal lesion is even more unusual. In this report, we present a patient with clear cell carcinoma occurring in the trachea, which obstructed the tracheal lumen and lead to the respiratory distress. PATIENT CONCERNS: A 60-year old female patient was admitted due to a 6-month history of dyspnea with worsening symptoms for 1 month. Chest CT scan revealed a smooth nodular shadow with homogeneous density on the wall of upper trachea. DIAGNOSIS: Bronchoscopy therapy and surgical removal of the tumor were performed. The histopathological diagnosis revealed clear cell carcinoma. INTERVENTION: Surgical removal of the clear cell carcinoma was performed. OUTCOMES: The patient recovered well after the surgery and is now being followed-up after hospital discharge. LESSONS: Bronchoscopy is an essential tool for diagnosis of tracheal clear cell carcinoma. Surgical removal should be performed if possible.