Zinc finger protein 367 exerts a cancer-promoting role in small cell lung cancer by influencing the CIT/LATS2/YAP signaling cascade.

A remarkable cancer-related role of zinc finger protein 367 (ZNF367) has been demonstrated in multiple malignancies. However, whether ZNF367 has a role in small-cell lung cancer (SCLC) remains unexplored. The purpose of this work was to explore the potential role and mechanism of ZNF367 in SCLC. In silico analysis using the Gene Expression Omnibus (GEO) dataset revealed high levels of the ZNF367 transcript in SCLC. Examination of clinical tissues confirmed the significant abundance of ZNF367 in SCLC tissues compared with adjacent non-malignant tissues. The genetic depletion of ZNF367 in SCLC cells led to remarkable alterations in cell proliferation, the cell cycle, colony formation and chemosensitivity. Mechanistically, ZNF367 was shown to regulate the activation of yes-associated protein (YAP) associated with the up-regulation of phosphorylated large tumour suppressor kinase 2 (LATS2). Further investigation revealed that ZNF367 affected the LATS2-YAP cascade by regulating the expression of citron kinase (CIT). Re-expression of constitutively active YAP diminished the tumour-inhibiting function of ZNF367 depletion. Xenograft experiments confirmed the tumour-inhibiting effect of ZNF367 depletion in vivo. In summary, our results demonstrate that the inhibition of ZNF367 displays anticancer effects in SCLC by inhibiting YAP activation, suggesting it as a potential druggable oncogenic target.

Associations between urbanization and the home language environment: Evidence from a LENA study in rural and peri-urban China.

In low- and middle-income countries, urbanization has spurred the expansion of peri-urban communities, or urban communities of formerly rural residents with low socioeconomic status. The growth of these communities offers researchers an opportunity to measure the associations between the level of urbanization and the home language environment (HLE) among otherwise similar populations. Data were collected in 2019 using Language Environment Analysis observational assessment technology from 158 peri-urban and rural households with Han Chinese children (92 males, 66 females) aged 18-24 months in China. Peri-urban children scored lower than rural children in measures of the HLE and language development. In both samples, child age, gender, maternal employment, and sibling number were positively correlated with the HLE, which was in turn correlated with language development.

The home language environment in rural China: variations across family characteristics.

BACKGROUND: A rich language environment is an important element of a nurturing home environment. Despite their proven importance, vocabulary and conversation have been shown to vary widely across households-even within the same socio-economic class. One significant gap in the existing literature is its nearly exclusive geographic focus on Western and developed settings, with little attention given to poorer communities in lower/middle income countries. The purpose of this study was to empirically illustrate the characteristics of the home language environment in the low SES, non-Western cultural setting of rural China. METHODS: Using Language Environment Analysis (LENA) automated language-analysis system, this study measured the home language environment of 38 children aged 20-27 months in Northwest rural China. Our primary measures of the home language environment were Adult Word Count (AWC), Conversational Turn Count (CTC) and Child Vocalization Count (CVC). Multivariate linear regression models were used to examine the association between home language environment and family/child characteristics, and language skills (Measured by MacArthur-Bates Communicative Developmental Inventory score). RESULTS: In this paper, by comparison, we found that the home language environment of our rural sample fell far behind that of urban households. We also identify significant, positive correlations between language skills and both AWC and CTC. Our analysis finds no significant correlations between home language environment and family/child characteristics. CONCLUSION: In this paper, we present the first ever findings using the LENA system to measure the home language environment of young children from poor rural communities in China. We found that the home language environment of lower-SES household was significantly worse than high-SES households, and demonstrated the importance of the home language environment to language skills, pointing to a need for more high-quality studies of the home language environment in rural China to better understand possible mechanisms behind low levels of parent-child language engagement and ways to improve the home language environment.

Family-level factors of early childhood development: Evidence from rural China.

Family-level factors that characterize the home environment are critical inputs to early language and cognitive development, and potential mechanisms for improving developmental outcomes in vulnerable populations. Many studies conducted in high-income and Western settings highlight stimulating parenting, the home language environment, and parental self-efficacy as possible mechanisms of early development, though less is known about how these family-level factors impact child development in low- or middle-income settings. Even less is known about these family-level factors and early childhood development in rural China, where rates of cognitive and language delay in children aged 0-3 years are as high as 45% and 46%, respectively. Using data collected from 77 rural households with children aged 18-24 months in Southwestern China, this study examines the associations between stimulating parenting, the home language environment, and parental self-efficacy, and early cognitive and language development. The results indicate that stimulating parenting was significantly associated with cognitive, language, and overall development; the home language environment was only significantly associated with language development; and parental self-efficacy was not significantly associated with any developmental outcomes. The implications of such findings reveal mechanisms for supporting healthy child development in rural China.

The home language environment and early language ability in rural Southwestern China.

Using premier Language Environment Analysis technology to measure and analyze the home language environment, this observational study aims to describe the home language environment and child language ability, drawing on empirical data from 77 households with children aged 18-24 months from rural China. The results show large variation in measures of the home language environment and early language ability, similar to other rural Chinese samples. Results also demonstrate significant correlations between child age and the home language environment, maternal employment and the home language environment, father's educational attainment and the home language environment, adult-child conversations and early language ability, and child vocalizations and early language ability.

Visual impairment in rural and migrant Chinese school-going children: prevalence, severity, correction and associations.

PURPOSE: To describe changes in the prevalence of visual impairment and glasses ownership with age and as associated with income and population density for visual impairment among rural and urban migrant Chinese students. DESIGN: Meta-analysis of 12 cross-sectional, school-based studies conducted between 2012 and 2017. SETTING: Rural and urban migrant schools in seven Chinese provinces. PARTICIPANTS: A total of 83 273 rural and urban migrant Chinese students aged 6-17 years. RESULTS: Prevalence of visual impairment (uncorrected visual acuity ≤6/12 in either eye) rose from 19.0% at age 6 to 66.9% at 17, with the overall age-adjusted prevalence higher for girls (35.8%) than for boys (30.1%, p<0.001). The rate of glasses ownership among students who needed them increased from 13.0% at age 6 to 63.9% (p<0.001) at 17 and was significantly higher for girls (37.0%) than boys (34.7%, p<0.001). The unmet need for glasses as a proportion of the student population peaked in junior high school (31.8%). A 1% increase in per capita gross domestic product was associated with a 4.45% rise in uncorrected visual acuity (R2=0.057, p=0.020). Population density was significantly associated with glasses ownership among children (R2=0.359, p=0.012). A 1% population density increase was associated with an increase in the glasses ownership rate of 6.83%. CONCLUSION: Efforts are needed to improve vision screening coverage in China's schools, particularly junior high schools, as this is when many rural children leave school and glasses coverage is lowest.

Circ_0046600 promotes hepatocellular carcinoma progression via up-regulating SERBP1 through sequestering miR-1258.

BACKGROUND: Circ_0046600 was reported to promote hepatocellular carcinoma (HCC) cell migratory ability. However, the functional roles and mechanism of circ_0046600 in HCC remain largely unknown. METHODS: Levels of genes and proteins were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. In vitro experiments were performed using cell counting kit-8 (CCK-8), colony formation, transwell, flow cytometry and Western blot assays, respectively. The direct interactions between miR-1258 and circ_0046600 or SERPINE1 mRNA-binding protein 1 (SERBP1) was verified using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenograft tumor model was established to perform in vivo assay. Exosomes were obtained from culture media by using the commercial kit. RESULTS: Circ_0046600 was highly expressed in HCC tissues and cells. Silencing of circ_0046600 impaired HCC cell growth and metastasis in vitro, as well as impeded HCC tumor growth in vivo. Mechanistically, circ_0046600 could competitively target miR-1258 to prevent the degradation of its target gene SERBP1. Rescue assay showed that miR-1258 inhibition reversed the inhibitory effects of circ_0046600 silencing on HCC cell. Moreover, ectopic overexpression of miR-1258 suppressed cell growth and metastasis in HCC, which was abolished by SERBP1 up-regulation. Furthermore, circ_0046600 was packaged into exosomes and could be derived from HCC cells. CONCLUSION: Circ_0046600 promoted HCC progression via up-regulating SERBP1 through sequestering miR-1258; besides that, circ_0046600 was packaged into exosomes and could be released from HCC cells.

Tumor Suppressor Gene XEDAR Promotes Differentiation and Suppresses Proliferation and Migration of Gastric Cancer Cells Through Upregulating the RELA/LXRα Axis and Deactivating the Wnt/ß-Catenin Pathway.

X-linked ectodermal dysplasia receptor (XEDAR) is a new member of the tumor necrosis factor receptor (TNFR) family that induces cell death. The purpose of this study is to determine the tumor-suppressive potential of XEDAR in the development and differentiation of gastric cancer (GC). XEDAR levels were analyzed in human GC tissues and adjacent normal tissues by immunohistochemistry (IHC), quantitative real-time reverse transcription PCR (RT-qPCR), and Western blot analysis. We found that XEDAR expression was significantly downregulated in GC tissues and further decreased in low differentiated GC tissues. Overexpression of XEDAR in MKN45 and MGC803 cells suppressed the ability of cell proliferation and migration, whereas silencing XEDAR showed the opposite effect. Additionally, XEDAR silencing resulted in the upregulation of the differentiation molecular markers ß-catenin, CD44 and Cyclin D1 at the protein levels, whereas XEDAR overexpression showed the opposite effect. Notably, XEDAR positively regulated the expression of liver X receptor alpha (LXRα) through upregulating the RELA gene that was characterized as a transcription factor of LXRα in this study. Inhibition of LXRα by GSK2033 or activation of the Wnt/ß-catenin pathway by Wnt agonist 1 impaired the effect of XEDAR overexpression on differentiation of MKN45 cells. Moreover, inhibition of RELA mediated by siRNA could promote cell proliferation/migration and rescue the effect of XEDAR overexpression on cell behaviors and expression of genes. Subsequently, overexpression of XEDAR suppressed the growth of GC cells in vivo. Taken together, our findings showed that XEDAR could promote differentiation and suppress proliferation and invasion of GC cells.

Impact of spectacles wear on uncorrected visual acuity among urban migrant primary school children in China: a cluster-randomised clinical trial.

OBJECTIVE: To estimate the effect of providing free spectacles on uncorrected visual acuity (VA) among urban migrant Chinese school children. DESIGN: Exploratory analysis from a parallel cluster-randomised clinical trial. METHODS: After baseline survey and VA screening, eligible children were randomised by school to receive one of the two interventions: free glasses and a teacher incentive (tablet computer if ≥80% of children given glasses were wearing them on un-announced examination) (treatment group) or glasses prescription and letter to parents (control group). The primary outcome was uncorrected logarithm of the minimal angle of resolution (LogMAR) VA at study closeout, adjusted for baseline uncorrected VA. RESULTS: Among 4376 randomly selected children, 728 (16.6%, mean age 10.9 years, 51.0% boys) at 94 schools failed VA screening and met eligibility criteria. Of these, 358 children (49.2%) at 47 schools were randomised to treatment and 370 children (50.8%) at 47 schools to control. Among these, 679 children (93.3%) completed follow-up and underwent analysis. Spectacle wear in the treatment and control groups was 68.3% and 29.3% (p<0.001), respectively. Uncorrected final VA for eyes of treatment children was significantly better than control children, adjusting only for baseline VA (difference of 0.039 LogMAR units, 95% CI: 0.008, 0.070, equivalent to 0.39 lines, p=0.014) or baseline VA and other baseline factors (0.040 LogMAR units, 95% CI 0.007 to 0.074, equivalent to 0.40 lines, p=0.020). CONCLUSION: We found no evidence that spectacles wear worsens children's uncorrected VA among urban migrant Chinese school children.

RP11­619L19.2 promotes colon cancer development by regulating the miR­1271­5p/CD164 axis.

Colon cancer (CC) is one of the leading causes of cancer­related mortality in China and western countries. Several studies have demonstrated that long non­coding RNAs (lncRNAs) play critical roles in cancer development. However, the function of lncRNA RP11­619L19.2 in colon cancer remains unclear. The aim of the present study was to investigate the expression pattern, function and underlying mechanism of action of RP11­619L19.2 in CC development and metastasis. RP11­619L19.2 was found to be highly expressed in CC tissues and cell lines, and it was associated with advanced TNM stage and lymph node metastasis. Furthermore, knockdown of RP11­619L19.2 inhibited CC cell proliferation, migration, invasion and epithelial­to­mesenchymal transition (EMT). It was also observed that RP11­619L19.2 was reciprocally repressed by miR­1271­5p. Of note, miR­1271­5p negatively regulated CD164 expression by directly targeting the 3'­untranslated region of CD164. Overexpression of CD164 reversed the antimetastatic activity of RP11­619L19.2 knockdown in CC cells. Mechanistically, it was demonstrated that lncRNA RP11­619L19.2 played an oncogenic role and promoted CC development and metastasis by regulating the miR­1271­5p/CD164 axis and EMT. In conclusion, the findings of the present study indicated that RP11­619L19.2 regulates CD164 expression and EMT by sponging miR­1271­5p, which may provide novel targets for lncRNA­directed diagnosis and therapy for patients with CC.

Safety of eyeglasses wear for visual acuity among middle school students in northwestern rural China: a cluster-randomised controlled trial.

OBJECTIVE: To assess the effect of free eyeglasses provision on visual acuity among middle school students in northwestern rural China. METHODS AND ANALYSIS: Among 31 middle schools randomly selected from 47 middle schools in northwestern rural China, students were randomly allocated by school to one of two interventions: free eyeglasses (intervention group), and eyeglasses prescriptions given only to the parents (control group). The main outcome of this study is uncorrected visual acuity after 9 months, adjusted for baseline visual acuity. RESULTS: Among 2095 students from 31 middle schools, 995 (47.5%) failed the visual acuity screening, 515 (51.8%, 15 schools) of which were randomly assigned to the intervention group, with the remaining 480 students (48.2%, 16 schools) assigned to the control group. Among these, a total of 910 students were followed up and analysed. Endline eyeglasses wear in the intervention group was 44%, and 36% in the control group. Endline visual acuity of students in the intervention group was significantly better than students in the control group, adjusting for other variables (0.045 LogMAR units, 95% CI 0.006 to 0.084, equivalent to 0.45 lines, p=0.027), and insignificantly better only for baseline visual acuity (difference of 0.008 LogMAR units, 95% CI -0.018 to 0.034, equivalent to 0.08 lines). CONCLUSION: We found no evidence that receiving free eyeglasses worsened visual acuity among middle school students in northwestern rural China. TRIAL REGISTRATION NUMBER: ISRCTN17141957.

Magnoflorine inhibits human gastric cancer progression by inducing autophagy, apoptosis and cell cycle arrest by JNK activation regulated by ROS.

The antitumor effect of magnoflorine (Mag), an alkaloid isolated from Coptidis Rhizoma, in gastric cancer (GC) cells has not been reported. In the study, Mag suppressed the proliferation of GC cells, but showed no influence on normal gastric cells. Mechanistically, Mag induced autophagy in GC cells, as evidenced by the up-regulated expression of LC3B-II and increased autophagosome formation. Furthermore, we found that Mag-triggered autophagic cell death was regulated by reactive oxygen species (ROS)-induced suppression of serine/threonine-protein kinases (AKT) signaling. What's more, Mag treatment led to apoptosis in GC cells through enhancing cleaved Caspase-3 and PARP expressions. In addition, up-regulated expression of p27 and p21, as well as down-regulated expression of Cyclin-A and Cyclin-B1 was detected in Mag-treated GC cells, contributing to the S/G2 cell cycle arrest. Importantly, Mag incubation resulted in a significant increase in jun N-terminal kinase (JNK) phosphorylation but not p38 and ERK1/2, which was involved in the modulation of apoptosis and S/G2 phase arrest. Moreover, ROS production was highly induced by Mag treatment, and Mag-exhibited these functions was largely dependent on the generation of ROS in GC cells. Consistently, the GC cell xenograft mouse model confirmed the anti-tumor role of Mag in vivo. Collectively, these results indicated that Mag showed anti-GC effects, which could be a potential therapeutic target for GC treatment.

RP5-1120P11.3 promotes hepatocellular carcinoma development via the miR-196b-5p-WIPF2 axis.

Hepatocellular carcinoma (HCC) remains a huge threat to human health even though the diagnosis and treatment strategies have improved rapidly in the past few decades. Increasing evidence has illustrated the critical role noncoding RNA and their regulatory network play in the pathology of HCC. Here, we identified a novel long noncoding RNA, RP5-1120P11.3, that is ectopically expressed in HCC. Further characterization of RP5-1120P11.3 revealed that it promoted proliferation and invasion of HCC cells while inhibiting apoptosis. Importantly, our data revealed that miR-196b-5p interacted with and was regulated by RP5-1120P11.3 via a sponging mechanism. Inhibition of miR-196b-5p attenuated the phenotypes resulting from RP5-1120P11.3 inhibition. Moreover, our data showed that miR-196b-5p inhibited the expression of WIPF2 in HCC, illustrating a regulatory axis of RP5-1120P11.3-miR-196b-5p-WIPF2 that facilitated the progression of HCC. In addition, our data showed that RP5-1120P11.3 contributed to xenograft generation in vivo by regulating miR-196b-5p and WIPF2. These findings suggested that the RP5-1120P11.3-miR-196b-5p-WIPF2 axis is a potential target for treatment of HCC.

Long Non-coding RNA LINC01420 Contributes to Pancreatic Cancer Progression Through Targeting KRAS Proto-oncogene.

BACKGROUND: Long non-coding RNAs (lncRNAs) have been increasingly uncovered to participate in multiple human cancers, including pancreatic cancer (PC). However, the underlying mechanisms of most of the lncRNAs have not been fully understood yet. AIMS: In this study, we probed the role and latent mechanism of LINC01420 in PC. METHODS: Several online tools were applied. Gene expression was evaluated by qRT-PCR or Western blot. Both in vitro and in vivo assays were conducted to probe LINC01420 function in PC. ChIP, RIP, and luciferase reporter assays were performed to determine relationships between genes. RESULTS: The bioinformatics analyses revealed LINC01420 was highly expressed in PC tissues. Besides, LINC01420 was pronouncedly upregulated in PC cell lines and its depletion controlled PC cell proliferation and EMT in vitro and hindered tumor growth in vivo. Importantly, KRAS was proved to mediate LINC01420-facilitated PC cell proliferation. Further, we explained that KRAS transcription was regulated by MYC, while LINC01420 enhanced the binding of MYC to KRAS promoter in the nucleus of PC cells. Intriguingly, LINC01420 boosted MYC expression in the cytoplasm of PC cells by sponging miR-494-3p. CONCLUSION: This study illustrated that LINC01420 accelerates PC progression through releasing miR-494-3p-silenced MYC in cytoplasm and upregulating MYC-activated KRAS in nucleus, unveiling LINC01420 as a latent therapeutic strategy for PC patients.

The long non-coding RNA HCG18 promotes the growth and invasion of colorectal cancer cells through sponging miR-1271 and upregulating MTDH/Wnt/ß-catenin.

Long non-coding RNAs (lncRNAs) have recently emerged as key regulators of the occurrence and progression of various human cancers, including colorectal cancer. However, the regulatory mechanism of lncRNAs in the tumorigenesis of colorectal cancer remains poorly understood. In this study, we aimed to elucidate the potential role of lncRNA HCG18 in colorectal cancer. Herein, we found that HCG18 expression was significantly upregulated in colorectal cancer tissues and cell lines. Knockdown of HCG18 significantly inhibited the growth and invasion of colorectal cancer cells, while its overexpression had the opposite effect. Moreover, HCG18 was identified as a sponge of miR-1271. Our results showed that knockdown of HCG18 markedly upregulated miR-1271 expression in colorectal cancer cells. Notably, HCG18 expression was inversely correlated with miR-1271 expression in colorectal cancer specimens. Further investigation revealed that HCG18 contributed to the enhancement of MTDH/Wnt/ß-catenin signalling in colorectal cancer cells. The antitumour effect of HCG18 inhibition was significantly reversed by miR-1271 inhibition or MTDH overexpression. Overall, the results of our study demonstrate that HCG18 exerts a potential oncogenic function in colorectal cancer by enhancing MTDH/Wnt/ß-catenin signalling via sponging of miR-1271, highlighting the importance of HCG18/miR-1271/ MTDH/Wnt/ß-catenin signalling in the progression of colorectal cancer.

Chicoric acid (CA) induces autophagy in gastric cancer through promoting endoplasmic reticulum (ER) stress regulated by AMPK.

Gastric cancer is one of the most common cancers leading to tumor-related deaths worldwide. Chicoric acid (CA) exhibits a variety of protective effects in different diseases. However, its role in regulating tumor progression has not been reported. Autophagy, as a conserved catabolic process, sustains cellular homoeostasis responding to stress to modulate cell fate. In the study, the effects of CA on gastric cancer were investigated. The results indicated that CA treatment markedly reduced the cell viability and induced apoptosis in gastric cancer cells, and prevented tumor growth in an established xenograft gastric cancer model. Furthermore, CA exposure significantly induced autophagy both in gastric cancer cells and tumor samples, as evidenced by the up-regulated expression of LC3II. Moreover, phosphorylated AMP-activated protein kinase (AMPK) and p70S6 kinase (p70s6k) expression were obviously promoted by CA in vitro and in vivo. Importantly, blocking AMPK activation abrogated CA-induced expression of LC3II in gastric cancer cells. In addition, endoplasmic reticulum (ER) stress in tumor samples or cells was markedly induced by CA treatment through promoting the expression of associated signals such as Parkin, protein kinase RNA-like ER kinase (PERK), activating transcription factors 4 (ATF4) and ATF6. Importantly, these effects were abolished by the inhibition of AMPK signaling. Collectively, our findings indicated that CA prevents human gastric cancer progression by inducing autophagy partly through the activation of AMPK, and represents an effective therapeutic strategy against gastric cancer development.

Myosin Heavy Chain-Associated RNA Transcripts Promotes Gastric Cancer Progression Through the miR-4529-5p/ROCK2 Axis.

BACKGROUND AND AIM: Characterization of genetic aberrations provides novel strategies for diagnosis and treatment of gastric cancer. Accumulating evidence has shown the involvement of long non-coding RNA (lncRNA) in the pathology of gastric cancer, especially in proliferation and metastasis. The aim of this study was to delineate the role of myosin heavy chain-associated RNA transcripts (MHRT), a heart-specific lncRNA, in gastric cancer and to understand the correlation between MHRT, miR-4529-5p, and ROCK2. METHODS: To study expression level of MHRT, clinical gastric cancer samples, gastric cancer cell lines, adjacent normal tissues, and gastric epithelial cell lines were used. Additionally, apoptosis, proliferation, and invasion of gastric cancer cells were studied with or without downregulation of MHRT and miR-4529-5p. RESULTS: We identified that MHRT was ectopically expressed in gastric cancer tissues and cell lines. Interestingly, similar to the anti-apoptotic role of MHRT in cardiomyocytes, our data illustrated that MHRT inhibits apoptosis of gastric cancer cells. Moreover, we found that MHRT promotes proliferation and invasion of gastric cancer cells in vitro. Importantly, our data revealed that MHRT regulates the expression of miR-4529-5p via direct binding. Additionally, functional experiments illustrated that miR-4529-5p is particularly responsible for MHRT-mediated regulation of apoptosis. Besides, ROCK2 was identified as a downstream target of miR-4529-5p. Additionally, upregulated MHRT promotes the expression of ROCK2 by inhibiting miR-4529-5p. CONCLUSION: Our data illustrated a MHRT/miR-4529-5p/ROCK2 regulatory axis that contributes to the tumorigenesis of gastric cancer and provided potential therapeutic targets for precise gastric cancer treatment.

A circular RNA derived from COL6A3 functions as a ceRNA in gastric cancer development.

Gastric cancer (GC) poses a serious threat to human life, whereas its pathogenesis remains elusive. The present study aimed to investigate the potential pathogenic mechanism behind gastric cancer development. RT-PCR analysis using divergent primers, RNase R digestion assay, and mRNA stability assay were performed to characterize circCOL6A3 (ID: hsa_circ_0006401) in GC cell lines; Western blot was conducted to detect the expression of COL6A3. Cell counting kit-8 (CCK-8), EdU incorporation assay, and Transwell were run to evaluate GC cell proliferation and migration. Luciferase reporter assay was performed to validate the relationship between miR-3064-5p and COL6A3. Both circCOL6A3 and COL6A3 were highly expressed in GC cells, while miR-3064-5p was down-regulated. Depleted circCOL6A3 significantly decreased cell viability and mobility, and increased cell apoptosis. CircCOL6A3 regulated the expression of miR-3064-5p, and the effect of si-circCOL6A3 on cell biological behaviors was abolished by miR-3064-5p inhibitor. MicroRNA-3064-5p targets COL6A3 to regulate its expression. Taken together, the present study indicated that overexpressed circCOL6A3 promoted cell proliferation, migration and apoptosis of gastric cancer through rescission of miR-3064-5p-induced inhibitory effect on COL6A3. Our study will furnish theoretical grounds for future clinical diagnosis and treatment of GC patients.

Knockdown of TMPRSS3 inhibits gastric cancer cell proliferation, invasion and EMT via regulation of the ERK1/2 and PI3K/Akt pathways.

The transmembrane protease, serine 3 (TMPRSS3), a member of the type II transmembrane serine protease family, plays an important role in mediating tissue development, homeostasis and various biological processes. Recently, TMPRSS3 has been reported to be involved in cancer progression. However, the role of TMPRSS3 in gastric cancer (GC) remains largely unknown. In this study, we found that TMPRSS3 was highly expressed in GC tissues and cell lines. Knockdown of TMPRSS3 inhibited GC cell proliferation, invasion and epithelial-mesenchymal transition (EMT) in vitro as well as suppressed GC cell growth and dissemination in vivo. These inhibitory effects were mediated by regulation of the ERK1/2 signaling pathway. Moreover, TMPRSS3-mediated ERK1/2 activation was dependent on the PI3K/Akt pathway. In conclusion, TMPRSS3 contributed to GC progression via activation of the PI3K/Akt/ERK signaling pathway and might act as a therapeutic target for GC treatment.

Probing excitons in transition metal dichalcogenides by Drude-like exciton intraband absorption.

Understanding excitonic dynamics in two-dimensional semiconducting transition metal dichalcogenides is important for developing their optoelectronic applications. Recently, transient absorption techniques based on resonant excitonic absorption have been used to study various aspects of excitonic dynamics in these materials. The transient absorption in such measurements originates from phase-space state filling, bandgap renormalization, or screening effects. Here we report a new method to probe excitonic dynamics based on exciton intraband absorption. In this Drude-like process, probe photons are absorbed by excitons in their intraband excitation to higher energy states, causing a transient absorption signal. Although the magnitude of the transient absorption is lower than that of the resonant techniques, the new method is less restrictive on the selection of probe wavelength, has a larger linear range, and can provide complementary information on photocarrier dynamics. Using the WS2 monolayer and bulk samples as examples, we show that the new method can probe exciton-exciton annihilation at high densities and reveal exciton formation processes. We also found that the exciton intraband absorption cross section of the WS2 monolayer is on the order of 10-18 cm2.