Epigenetic regulation of autophagy by non-coding RNAs and exosomal non-coding RNAs in colorectal cancer: A narrative review.

One of the major diseases affecting people globally is colorectal cancer (CRC), which is primarily caused by a lack of effective medical treatment and a limited understanding of its underlying mechanisms. Cellular autophagy functions to break down and eliminate superfluous proteins and substances, thereby facilitating the continual replacement of cellular elements and generating vital energy for cell processes. Non-coding RNAs and exosomal ncRNAs have a crucial impact on regulating gene expression and essential cellular functions such as autophagy, metastasis, and treatment resistance. The latest research has indicated that specific ncRNAs and exosomal ncRNA to influence the process of autophagy in CRC cells, which could have significant consequences for the advancement and treatment of this disease. It has been determined that a variety of ncRNAs have a vital function in regulating the genes essential for the formation and maturation of autophagosomes. Furthermore, it has been confirmed that ncRNAs have a considerable influence on the signaling pathways associated with autophagy, such as those involving AMPK, AKT, and mTOR. Additionally, numerous ncRNAs have the potential to affect specific genes involved in autophagy. This study delves into the control mechanisms of ncRNAs and exosomal ncRNAs and examines how they simultaneously influence autophagy in CRC.

Effects of biochar application methods on greenhouse gas emission and nitrogen use efficiency in paddy fields.

Biochar application in rice production reduces nitrogen loss and greenhouse gases. We conducted in situ experiments for 3 years, with N210B0 (210 kg N ha-1) as the control. Two biochar application methods (B1:15 t ha-1 biochar applied once and B2: biochar applied three times at 5 t ha-1 yr-1) combined with two nitrogen levels (N210: 210 kg N ha-1 and N168: 168 kg N ha-1) were used. Soil physicochemical properties, CH4 and N2O emissions, functional gene abundance, rice yield, and nitrogen use efficiency were analyzed. Both methods improved the physicochemical properties of the soil, however, B1 was less effective than B2 in increasing soil pH, bulk density, organic carbon, total nitrogen, and microbial biomass nitrogen in year 3. B1 had a higher CH4 emission mitigation effect than B2 in 3 consecutive years, mainly due to the higher pmoA gene abundance. B1 showed a higher reduction effect of N2O emissions compared to B2 in year 1, but the opposite was observed in years 2 and 3. B2 had a higher abundance of AOB, nirK, and nosZ genes compared to B1 in year 3. Compared with N210B0, rice yields were increased by 9.1 %, 9.6 %, and 3.6 % with N210B1, N210B2, and N168B2, respectively, over 3 years, while N168B1 improved yields in the previous 2 years. Biochar improved nitrogen use efficiency over 3 consecutive years directly due to increased use efficiency of panicle fertilizer; the effect of B1 was greater than that of B2 during years 1 and 2, while the opposite was observed in year 3. Both Biochar applied once and three times appeared to be promising practices to increase yield and mitigate GHGs. From the GHGI perspective, the biochar applied once combined with 168 kg N ha-1 can further improve nitrogen use efficiency, and reduce GHGs without hindering improvements in rice yield.

RNA­binding protein quaking 5 inhibits the progression of non­small cell lung cancer by upregulating netrin­4 expression.

It was recently reported that netrin­4 (Ntn­4), a component of the extracellular matrix, when downregulated, is involved in the progression of several types of cancer, including breast cancer, colorectal tumours, neuroblastoma and gastric cancer. In the present study, the level of Ntn­4 was examined in a public non­small cell lung cancer (NSCLC) dataset from the Netherlands Cancer Institute. This analysis revealed that the mRNA expression level of Ntn­4 was lower in the samples of patients with NSCLC compared with that in the control samples. Consistent with the mRNA level, the protein level of Ntn­4 was also found to be decreased in NSCLC cells. However, both the function of Ntn­4 and the underlying mechanisms of Ntn­4 downregulation in NSCLC have yet to be fully elucidated. As was anticipated, the overexpression of Ntn­4 led to a marked decrease in the proliferation, migration and invasion of NSCLC cells. Notably, RNA­binding protein quaking 5 (Qki­5) was found to exhibit antitumor activity in lung cancer, not only by enhancing the level of Ntn­4 by binding to Ntn­4 mRNA, but also by suppressing the proliferation, invasion and migration of NSCLC cells. However, Qki­5 is known to be frequently downregulated in NSCLC. Moreover, the knockdown of Ntn­4 was found to reverse the suppressive effects of Qki­5 on NSCLC progression both in vitro and in vivo. Taken together, the findings of the present study demonstrate that Ntn­4 is able to suppress the progression of NSCLC, and that the level of Ntn­4 can be regulated by Qki­5. Therefore, Ntn­4 may be a novel diagnostic and therapeutic target for the treatment of NSCLC.

A novel variant in BCL11B in an individual with neurodevelopmental delay: A case report.

BACKGROUND: B-Cell CLL/Lymphoma 11B (BCL11B) is a C2 H2 zinc finger transcription factor that has broad biological functions and is essential for the development of the immune system, neural system, cardiovascular system, dermis, and dentition. Variants of BCL11B have been found in patients with neurodevelopmental disorders and immunodeficiency. MATERIALS AND METHODS: Whole-exome sequencing (WES) and clinical examinations were performed to identify the etiology of our patient. A variant in the BCL11B gene, NM_138576.4: c.1206delG (p.Phe403Serfs*2) was found and led to frameshift truncation. RESULTS: We reported a male patient with developmental delay and cerebral palsy who carried the BCL11B variant. The detailed clinical features, such as brain structure and immune detection, were described and reviewed in comparison to previous patients. CONCLUSIONS: The BCL11B-related neurodevelopmental disorders are rare, and only 17 variants in 25 patients have been found to date. Our report expands the variants spectrum of BCL11B and increases the case of neurodevelopmental abnormalities.

Apolipoprotein A-I mimetic peptides (ApoAI MP) improve oxidative stress and inflammatory responses in Parkinson's disease mice.

Purpose: Parkinson's disease (PD) is closely associated with oxidative stress and inflammatory situation. Apolipoprotein A-I mimetic peptides (ApoAI MP) have antioxidant and anti-inflammatory properties. We aimed to study the therapeutic effect of ApoAI MP on PD mice, and to explore the related mechanisms. Methods: PD mice were induced by using 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP). The model mice were treated with different concentrations of ApoAI MP. The open-field behavioral test assesses the total distance moved, the rest time, and the number of crossings and Rota-rod was used to evaluate motor coordination. Oxidative stress was identified by measuring the levels of superoxide dismutase (SOD), catalase (CAT), glutathionperoxidase (GSH-Px), malondialdehyde, ROS and H2O2. Inflammatory situation was analyzed by measuring the levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6). Meanwhile, the scavenging activities of ApoAI MP for ABTS, DPPH, hydroxyl radical and superoxide anion, and the effects of the peptide on neurotransmitters were evaluated. Results: PD model establishment increased oxidative stress and inflammatory status by increasing the concentrations of ROS and H2O2 production, and the levels of TNF-α, IL-1ß and IL-6 (p < 0.05). ApoAI MP intervention improved PD symptoms by reducing the total moved distance and the number of passes (p < 0.01), and the falling times from Rota-rod, and increasing rest time (p < 0.05). ApoAI MP increased antioxidant properties by increasing the activities of SOD, CAT and GSH-Px, and reducing MDA concentration (p < 0.05). ApoAI MP addition reduced oxidative stress by scavenging ABTS, DPPH, hydroxyl radicals and superoxide anion and reducing the concentrations of ROS and H2O2 production (p < 0.05). ApoAI MP treatment increased anti-inflammatory capacities by reducing the concentrations of TNF-α, IL-1ß and IL-6 (p < 0.05). HPLC analysis showed that the peptide treatment improved neurotransmitters. Conclusion: ApoAI MP can improve the behavioral performance of PD mice by improving antioxidant and anti-inflammatory capacities.

LINC01094/SPI1/CCL7 Axis Promotes Macrophage Accumulation in Lung Adenocarcinoma and Tumor Cell Dissemination.

Objective: Infiltration of tumor-associated macrophages is closely linked to the malignant development of human cancers. This research studies the function of C-C motif chemokine ligand 7 (CCL7) in the macrophage accumulation in lung adenocarcinoma (LUAD) and the underpinning mechanism. Methods: The expression profile of CCL7 in LUAD and its correlations with patient's prognosis and macrophage infiltration were predicted via bioinformatics systems. Artificial up- or downregulation of CCL7 was induced in LUAD cells to explore its function in the mobility, EMT of cancer cells, and migration of M2 macrophages. Cancer cells were implanted in NOD/SCID mice to induce xenograft tumors. The CCL7-related transcription factors or factors were predicted by bioinformatic tools, and the molecular interactions were confirmed by immunoprecipitation or luciferase assays. Results: CCL7 was highly expressed in LUAD and linked to increased TAM infiltration. Knockdown of CCL7 suppressed the chemotaxis and M2 skewing of macrophages, and it blocked the EMT and mobility of LUAD cells. CCL7 downregulation also suppressed macrophage infiltration in xenograft tumors in mice. Spi-1 proto-oncogene (SPI1) was confirmed as an upstream factor activating CCL7 transcription, and LINC01094 was found to bind to SPI1 to promote its nuclear translocation. Upregulation of SPI1 restored the chemotactic migration and M2 polarization of macrophages in LUAD cells. Conclusion: This paper reveals that LINC01094 binds to SPI1 to promote its nuclear translocation, which further activates CCL7 transcription by binding to its promoter, leading to M2 macrophage accumulation and dissemination of tumor cells.

Prevalence of and factors associated with unintended pregnancies among sexually active undergraduates in mainland China.

BACKGROUND: Unintended pregnancies (UIP) among unmarried sexually active college students in mainland China have emerged as a major reproductive health issue with detrimental personal and socioeconomic consequences. This cross-sectional study aimed to determine the prevalence and factors associated with UIP among sexually active undergraduates in mainland China. METHODS: Between September 8, 2019 and January 17, 2020, a total of 48,660 participants were recruited across the Chinese mainland to complete the self-administered, structured, online questionnaire. This analysis was restricted to 6347 sexually experienced, never-married 15-26 year old undergraduates. Pearson's Chi square tests and multivariate Logistic regression analyses were performed to identify sociodemographic, familial and individual variables associated with UIP. RESULTS: The overall prevalence of UIP was 17.7%. More specifically, 19.5% of male college students reported they had unintentionally gotten a partner pregnant, while 14.9% of female college students became unintentionally pregnant. Students who experienced UIP were more likely to belong to the older age group (23-26 years), live with only one parent or live without parents at home, report that their family members approve of premarital sex, initiate sexual activity younger than 14 years old and have casual sex partners. Furthermore, females with multiple partners and males who came from low- income households, experienced sexual abuse, perceived difficulties in acquiring condoms and did not know how to use condoms correctly were also at higher risk of experiencing an unintended pregnancy. CONCLUSION: In order to prevent UIP, a comprehensive intervention measure should be taken to target older students and those engaging in risky sexual behaviors, work with young male students to improve condom use skills, improve the availability of free condoms, optimize the involvement of parents and other family members in their children's sex education.

In this study, we aimed to determine the prevalence and factors associated with UIP among sexually active undergraduates in mainland China. Between September 8, 2019 and January 17, 2020, a total of 48,660 participants were recruited from the Chinese mainland to complete the self-administered, structured, online questionnaire. This analysis was restricted to 6347 sexually experienced, never-married 15­26 year old undergraduates. Based on a social-ecological theoretical framework, we ran separate multivariate Logistic regression models for men and women to identify sociodemographic, familial and individual variables associated with UIP. Our findings indicate that the overall prevalence of UIP was 17.7%. More specifically, 19.5% of male college students reported they had unintentionally gotten a partner pregnant, while 14.9% of female college students became unintentionally pregnant. Students who experienced UIP were more likely to belong to the older age group, live with only one parent or live without parents at home, report that their family members approve of premarital sex, initiate sexual activity younger than 14 years old and have casual sex partners. Furthermore, females with multiple partners and males who came from low-income households, experienced sexual abuse, perceived difficulties in acquiring condoms and did not know how to use condoms correctly were also at higher risk of having an unintended pregnancy. In order to prevent UIP, a comprehensive intervention measure should be taken to target older students and those engaging in risky sexual behaviors, work with young male students to improve condom use skills, improve the availability of free condoms, optimize the involvement of parents and other family members in their children's sex education.

A circular RNA derived from FAT atypical cadherin 3 promotes lung cancer progression via forming a regulatory loop with oncogenic ELAV like RNA binding protein 1.

Circular RNA (circRNA) is a covalently closed endogenous RNA that participates in disease progression. However, its role in lung cancer is largely undetermined. In the present study, we found an onctogenic circRNA in lung cancer, FAT atypical cadherin 3 (FAT3) circRNA (circ-FAT3) was remarkably upregulated in lung cancer in comparison to paired normal tissues. High circ-FAT3 was closely linked to larger tumour size, lymph node metastasis, later clinical stage, as well as dismal outcome. Stable knockdown of circ-FAT3 inhibited cell proliferation and metastasis both in vitro and in vivo. RNA binding protein ELAV like RNA binding protein 1 (HuR) was found to bind to introns flanking circ-FAT3, promoting the cyclization and generation of circ-FAT3. Further, circ-FAT3 was able to sponge miR-136-5p by acting as a competing endogenous RNA (ceRNA), alleviating the repressive effect of miR-136-5p on HuR mRNA at the transcriptional and post-transcriptional levels. Moreover, circ-FAT3 expression in lung cancer tissues was strongly positively and negatively correlated with HuR and miR-136-5p expression, respectively. Overall, our data reveal the previously uncharacterized regulatory loop of circ-FAT3/miR-136-5p/HuR in lung cancer and provide novel evidence for the importance of circRNA as a ceRNA in tumorigenesis.

The expression and correlation between chemokine CCL7 and ABCE1 in non-small cell lung cancer.

Lung cancer is a malignant disease, and has the highest incidence and mortality worldwide. Lung cancer is also a popular subject in the field of cancer research. The molecular mechanisms of lung cancer development, invasion and metastasis need to be determined to prolong survival times and improve the quality of life. Recent studies have demonstrated that ATP-binding cassette sub-family E member 1 (ABCE1) is one of the factors that contributes to the development and metastasis of lung cancer, but the specific mechanism of this phenomenon remains unclear. A polymerase chain reaction microarray was used in the present study to screen for chemokine (C-C motif) ligand 7 (CCL7) expression in cell lines that highly expressed ABCE1, and the results showed that CCL7 was highly expressed in H1299 cells (P<0.01). The expression of CCL7 and ABCE1 in lung cancer tissues obtained from 30 patients with non-small cell lung cancer (NSCLC) was higher than that in adjacent normal lung tissues (P<0.01), and a positive correlation between the expression levels of the two genes in NSCLC was observed. These findings indicate that ABCE1 is involved in the development and progression of lung cancer through the CCL7 signaling pathway.

Adverse Effects of Hydroalcoholic Extracts and the Major Components in the Stems of Impatiens balsamina L. on Caenorhabditis elegans.

Impatiens balsamina L. (Balsaminaceae), an annual herb found throughout China, has been extensively used in traditional Chinese medicine (TCM). However, our knowledge regarding the adverse effects of I. balsamina in vivo is very limited. In this present study, the nematode Caenorhabditis elegans model was employed to fully assess the adverse effects of hydroalcoholic (EtOH 55%) extracts of I. balsamina stems (HAEIBS) in vivo. After exposure to 10 mg/mL HAEIBS, the major organism-level endpoints of C. elegans of percent survival, frequency of head thrash and body bends, and reproduction had decreased by 24%, 30%, and 25%, respectively. The lifespan of C. elegans was also greatly reduced after HAEIBS exposure compared to the controls. The active compounds in HAEIBS were separated using high speed countercurrent chromatograph (HSCCC) and characterized by high performance liquid chromatography (HPLC) and nuclear magnetic resonance (NMR). Two compounds, lawsone and 2-methoxy-1,4-naphthoquinone (MNQ), and their adverse effects were then more thoroughly detailed in this study. It was found that lawsone is the major toxin in HAEIBS with a higher toxicity than MNQ in terms of negative impact on C. elegans mortality, locomotion, reproduction, and lifespan. Our data also suggests that the C. elegans model may be useful for assessing the possible toxicity of other Chinese medicines, plant extracts, and/or compounds.

Effects of maslinic acid on the proliferation and apoptosis of A549 lung cancer cells.

Maslinic acid (MA) is a pentacyclic triterpene acid that is present in numerous dietary plants. Although certain studies have demonstrated that MA has anti­cancer properties in different cell types, the effect of MA on lung cancer cell proliferation and apoptosis and the potential underlying mechanisms remain to be elucidated. In the present study, A549 lung cancer cells were treated with different doses of MA and it was found that MA significantly inhibited A549 cell growth in a dose­dependent manner. In addition, Annexin V/propidium iodide flow cytometric analysis demonstrated that MA induced apoptosis of A549 cells. The present study also confirmed that MA induced apoptosis by observing morphological alterations. In addition, the effect of MA treatment on the levels of apoptosis­associated proteins was examined. The results demonstrated that MA treatment suppressed the expression of caspase­3, ­8 and ­9, and increased the expression of cleaved caspase­3, ­8 and ­9 in a dose­dependent manner. The level of inhibitors of apoptosis (IAPs) and Smac, which are possible upstream factors of caspase proteins, were also examined. It was found that MA treatment increased the protein expression of Smac and decreased the protein levels of c­IAP1, c­IAP2, X­linked inhibitor of apoptosis protein (XIAP) and Survivin in a dose­dependent manner. These results suggested that MA inhibited proliferation and induced apoptosis of A549 cells through regulation of caspase cleavage as well as Smac, c-IAP1, c-IAP2, XIAP and Survivin.

A new anthraquinone from seed of Cassia obtusifolia.

Seeds of Cassia obtusifolia L. are known as homology of medicine and food material, which is a commonly consumed beverage in China. One new compound, 8-hydroxy-1,7-dimethoxy-3-methylanthracene-9,10-dione-2-O-ß-d-glucoside (1), together with 11 known compounds, including seven anthraquinones (2-8), was isolated from the seeds. The 2D NMR data of compound 2 are reported for the first time. The structures of the compounds were established on the basis of 1D and 2D NMR, IR and HR-ESI-MS spectra. The cytotoxic activities of all the compounds against five cell lines (LO2, HCT-116, A549, HepG2 and SGC7901) were evaluated by using CCK8 methods. Compounds 1, 3 and 7 show moderate cytotoxicity towards HCT-116 cells compared with oxaliplatin.

LRRC3B is downregulated in non-small-cell lung cancer and inhibits cancer cell proliferation and invasion.

LRRC3B has emerged as a tumor suppressor in several human cancers. However, its expression pattern and biological roles in human non-small-cell lung cancer (NSCLC) have not been explored. In the present study, we investigated clinical significance of LRRC3B in 101 NSCLC specimens. We found that LRRC3B expression was downregulated in NSCLC tissues compared with normal bronchial epithelium and that its downregulation significantly correlated with tumor-node-metastasis (TNM) stage (p < 0.0001), nodal metastasis (p < 0.0001), and poor patient prognosis (p = 0.0016, log-rank test). We also checked LRRC3B levels in several lung cancer cell lines and found that its expression was downregulated in four of nine lung cancer cell lines compared with normal human bronchial epithelial (NHBE) cell line. We further explored the biological role of LRRC3B. LRRC3B plasmid transfection in H460 and A549 cell lines inhibited proliferation, colony formation ability, and invading ability. Furthermore, we identified that LRRC3B could inhibit cell cycle progression with downregulation of cyclin D1 and decreased MMP9 expression. In addition, LRRC3B depletion in HBE cells promoted proliferation and invasion. In conclusion, our data suggested that LRRC3B may serve as an important tumor suppressor in NSCLC.

Inflammation and pathological damage to the lungs of mice are only partially reversed following smoking cessation on subacute exposure to cigarette smoke.

The present study aimed to observe the level of inflammation and the number of lesions in the airways and parenchyma of mouse lungs subsequent to smoking cessation following 4 weeks exposure to cigarette smoke. Enlargement of the regional airspaces, deposition of peribronchial collagen fibers and macrophage infiltration were assessed. In addition, the expression levels of matrix metalloproteinase (MMP)­12 and transforming growth factor (TGF)­ß1 were detected in the airways and lung parenchyma of C57BL/6 J mice. Mice, which were exposed to filtered air for 4 weeks or cigarette smoke for 8 weeks were used as control groups. A 4 week duration of smoke exposure induced the expansion of alveolar spaces ~100 µm from the terminal bronchioles, but without increased deposition of collagen around the small airways, which was not reversed following smoking cessation. Pulmonary infiltration of macrophages and the protein expression levels of MMP­12 and TGF­ß1 increased in the airways following 4 weeks smoke exposure, however, there was no further increase at 8 weeks, and the expression levels of TGF­ß1 in the lung parenchyma decreased. At 4 weeks post­smoking cessation, the expression levels of TGF­ß1 in the airways and lung parenchyma returned to normal; whereas, 1 week after smoking cessation, the expression levels of MMP­12 were higher compared with the normal control group. Subacute exposure to cigarette smoke induced an inflammatory response and regional damage to the lung parenchyma, prior to deposition of collagen around the airways. Following smoking cessation, the pulmonary inflammatory reaction was partially reversed, however, macrophage infiltration and the expression levels of MMP­12 remained significantly higher compared with the control mice. These results suggested that regulation of the expression of MMP­12 and TGF­ß1, particularly in the distribution in the airways and lung parenchyma, may be a strategy for the early treatment of chronic obstructive pulmonary disease.

RNA interference-mediated knockdown of RhoGDI2 induces the migration and invasion of human lung cancer A549 cells via activating the PI3K/Akt pathway.

Rho GDP dissociation inhibitor 2 (RhoGDI2) has been identified as a tumor suppressor gene for cellular migration and invasion. However, the underlying mechanism and effector targets of RhoGDI2 in lung cancer are still not fully understood. In this study, a vector-expressed small hairpin RNA (shRNA) of RhoGDI2 was transfected into the human lung cancer cell line A549. After the successful transfection, the down-regulation of RhoGDI2 promoted the proliferation, migration, and invasion of lung cancer cells in vitro through the increasing expression and activities of the matrix metallopeptidase 9 (MMP-9) and PI3K/Akt pathways. Transiently transfecting the small interfering RNA (siRNA) of MMP-9 into the RhoGDI2 shRNA cells reduced the MMP-9 expression. Both transfecting the siRNA and adding the MMP-9 antibody into the RhoGDI2 shRNA cells led to a decrease in the invasion and migration of the lung cancer cells. The blockade of the PI3K/Akt pathway by LY294002 resulted in abolishment of the effects of RhoGDI2 shRNA in Akt phosphorylation and MMP-9 expression. This result suggests that the down-regulated RhoGDI2 contributed to the migration and invasion of the lung cancer cell line via activating the PI3K/Akt pathway and the ensuing increase in the expression and activity of MMP-9. In conclusion, we report that the shRNA-mediated knockdown of RhoGDI2 induces the invasion and migration of lung cancer due to cross-talk with the PI3K/Akt pathway and MMP-9. Verifying the role and molecular mechanism of the participation of RhoGDI2 in the migration and invasion of lung cancer may provide a target for better treatment.

[Steroidal Glycoside Constituents from Solanum cumingii].

OBJECTIVE: To investigate the steroidal glycoside constituents of Solanum cumingii. METHODS: The compounds were isolated by silica gel, Sephadex LH-20, RP-C18 column and Pre-HPLC chromatography. Their structures were identified by ESI-MS and NMR. RESULTS: Six known compounds including torvoside K (1), torvoside J (2), torvoside L (3), khasianine (4), aculeatiside A (5) and solamargine (6) were isolated from Solanum cumingii. CONCLUSION: All compounds are isolated from Solanum cumingii for the first time.

Acidically oxidized carbon cloth: a novel metal-free oxygen evolution electrode with high catalytic activity.

The efficiency of many energy storage technologies is limited by the sluggish kinetics of the oxygen evolution reaction (OER) and it is thus of great importance to develop highly active OER electrocatalysts made from earth-abundant elements. In this communication, we report a novel metal-free oxygen evolution electrode with high catalytic activity and stability through simple acidic oxidation of commercially available carbon cloth (CC). The resulting acidically oxidized CC exhibits an overpotential of 328 mV and a Tafel slope of 82 mV dec(-1) with 100% Faradaic efficiency. This electrode needs an overpotential of 477 mV to afford a current density of 10 mA cm(-2) and maintains its catalytic activity for at least 24,000 s. It offers us a low-cost flexible electrocatalytic electrode for device integration toward water splitting and rechargeable metal-air battery applications.

Effect of daphnoretin on the proliferation and apoptosis of A549 lung cancer cells in vitro.

Daphnoretin is an active constituent of Wikstroemia indica C.A. Mey., which is widely distributed in the northwest and southwest regions of China. Previous studies have shown that daphnoretin has anticancer effects on leukemia, osteosarcoma and uterine cervix cancer cells. However, the effect of daphnoretin on human lung cancer cells has yet to be elucidated. In the present study, daphnoretin was observed to inhibit A549 lung cancer cell proliferation in a concentration- and time-dependent manner. Fluorescent microscopy and flow cytometric analysis showed that daphnoretin induced A549 cell apoptosis in a concentration-dependent manner. Western blot analysis also revealed that daphnoretin induced apoptosis through the regulation of the B-cell lymphoma-2 gene family in A549 cells. These findings indicate that daphnoretin may have potential as a therapeutic agent for the management of lung cancer.

20-(s)-ginsenoside Rg3 induces apoptotic cell death in human leukemic U937 and HL-60 cells through PI3K/Akt pathways.

Leukemia is currently one of the most deadly diseases. Ginseng has been used in Asian countries for the treatment and prevention of various diseases, including leukemia, but the molecular mechanism of its antileukemia activity has not been well defined. The aim of this study was to explore the effect of 20-(s)-ginsenoside Rg3 on apoptosis in human leukemic U937 and HL-60 cells and the underlying mechanism. We found that 20-(s)-ginsenoside Rg3 reduced cell viability and induced apoptosis in U937 and HL-60 cells. The induction of apoptosis was accompanied by the downregulation of PI3K/Akt family proteins. Moreover, we observed that 20-(s)-ginsenoside Rg3 treatment resulted in activation of caspase-3 and caspase-9. Taken together, our findings suggest for the first time that 20-(s)-ginsenoside Rg3 can promote apoptosis in U937 and HL-60 cells, at least partly through the downregulation of PI3K/Akt family proteins. Moreover, the triggering of caspase-3 and caspase-9 activation mediated apoptotic induction. All these findings collectively demonstrate that the natural compound 20-(s)-ginsenoside Rg3 effectively induces apoptosis in human leukemic cells, which suggests that this compound may play a role in future therapies for leukemia.