[Genetic analysis of a fetus with Meckel syndrome due to variants of TMEM67 gene].

OBJECTIVE: To carry out prenatal diagnosis for a fetus with Meckel syndrome (MKS) and explore its genetic basis. METHODS: A pregnant woman presented at Suzhou Municipal Hospital in February 2018 was selected as the study subject. Clinical data was collected. Muscle tissue sample from the abortus and peripheral blood samples from the couple were collected. Genomic DNA was extracted and subjected to chromosomal microarray analysis (CMA) and whole exome sequencing. Candidate variant was verified by Sanger sequencing. RESULTS: The fetus was found to have microcephaly, oligohydramnios, polycystic kidneys and banana-shaped cerebellum at 18 weeks of gestation. After induction of labor, it was found to have encephalocele, renal cysts and polydactyly. CMA has found no abnormality. Whole exome sequencing revealed novel compound heterozygous variants c.296delA (p.Lys99SerfsTer6) and c.1243G>A (p.Val415Met) in the TMEM67 gene. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), the c.296delA variant was predicted to be pathogenic (PVS1+PM2_Supporting+PP4), whilst the c.1243G>A variant was predicted to be likely pathogenic (PM2_Supporting+PM3+PP3_Moderate+PP4). CONCLUSION: The c.296delA and c.1243G>A compound heterozygous variants of the TMEM67 gene probably underlay the MKS in this fetus.

Association of three missense mutations in the homocysteine-related MTHFR and MTRR gene with risk of polycystic ovary syndrome in Southern Chinese women.

BACKGROUND: The etiology between homocysteine and polycystic ovary syndrome (PCOS) is unclear. In humans, the level of homocysteine is mainly affected by two enzymes: methylene tetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR). While the activity of these two enzymes is mainly affected by three missense mutations, namely C677T (MTHFR), A1298C (MTHFR), and A66G (MTRR). This study aims to examine the association between the three missense mutations and PCOS and investigate whether the three missense mutations exerted their effect on PCOS by affecting the homocysteine level. METHODS: A case-control study was designed, comprising 150 people with PCOS and 300 controls. Logistic regression analysis was used to assess the association between the three missense mutations and PCOS. Linear regression analysis was used to assess the association between the three missense mutations and the homocysteine level. Mediation analysis was used to investigate whether the three missense mutations exerted their effect on PCOS by affecting the homocysteine level. RESULTS: Following adjustments and multiple rounds of testing, MTHFR A1298C was found to be significantly associated with PCOS in a dose-dependent manner (compared to AA, OR = 2.142 for AC & OR = 3.755 for CC; P < 0.001). MTRR A66G was nominally associated with PCOS. Mutations in MTHFR A1298C and MTRR A66G were significantly associated with the homocysteine level. Mediation analysis suggested the effect of MTHFR A1298C on PCOS was mediated by homocysteine. CONCLUSIONS: MTHFR A1298C and MTRR A66G were associated with PCOS, and MTHFR A1298C might affect the risk of PCOS by influencing the homocysteine level.

Development of a highly thermostable immunoassay based on a nanobody-alkaline phosphatase fusion protein for carcinoembryonic antigen detection.

Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM-5) assays are employed in routine clinical settings to diagnose tumor. We selected two nanobodies with high-affinity to CEACAM-5, termed Nb11C12 and Nb2D5, using phage-display technology. The Nb2D5 fused with calf intestinal alkaline phosphatase (CAP), human placental alkaline phosphatase (HAP), or Pyrococcus abyssi alkaline phosphatase (PAP) were expressed in human embryonic kidney (HEK293) cells. The enzymatic activity of Nb2D5-HAP fusion protein was the best and remained stable at 60 °C for 7 days. The affinity of Nb2D5-HAP fusion protein to CEACAM-5 reached 42 pM. A chemiluminescent enzyme immunoassay (CLEIA) based on Nb2D5-HAP fusion protein was established for quantitative CEACAM-5 assay in clinical settings. The CLEIA exhibited a wide linear range of 0.31-640 ng/mL toward CEACAM-5, with a limit of detection (LOD) of 0.85 ng/mL. No cross-reactivity occurred with CEACAM-1, CEACAM-3, CEACAM-6, or CEACAM-8, and no interference was observed with rheumatoid factors. The CLEIA based on Nb2D5-HAP fusion protein was stable for 8 weeks at 37 °C and 50% relative humidity. The CLEIA developed from Nb2D5-HAP fusion protein had much better stability and linearity with similar reproducibility compared with the enzyme-linked immunosorbent assay developed from conventional monoclonal antibodies, which have been widely used in clinics over the past several decades. Graphical abstract.

[Prenatal diagnosis of a fetus with cleft lip and palate by using chromosomal microarray analysis].

OBJECTIVE: To explore the genetic basis for a fetus with cleft lip and palate. METHODS: Copy number variations (CNVs) in the fetus and his parents were detected with chromosomal microarray analysis (CMA). RESULTS: As revealed by the CMA assay, the fetus has carried a 228 kb deletion in Xp11.22 region and a 721 kb duplication in 9p21.1. Both CNVs were inherited from the parents. The CNV in Xp11.22 was predicted to be pathogenic by involving the PHF8 gene, whilst the CNV in 9p21.1 was predicted to be benign. CONCLUSION: Deletion of the Xp11.22 region probably underlies the cleft lip and palate in this fetus.

Combining the Advantages of Alkene and Azo E-Z Photoisomerizations: Mechanistic Insights into Ketoimine Photoswitches.

We carried out CASPT2//(TD)DFT and CASPT2//CASSCF studies on the working mechanism of imine switches, including a camphorquinone-derived ketoimine (shortened as k-Imine) switch designed by Lehn as well as a model camphorquinone alkene-imine (a-Imine) proposed in this study. Under the experimental conditions (light irradiation with 455 and 365 nm for E and Z, respectively), k-Imine is excited to the S1:(nN,π*) state and then decays toward a perpendicular intermediate following the C═N bond rotation coordinate. During the bond rotation, a mild energy barrier caused by the strong interaction of S1:(nN,π*) and S2:(nO,π*) states will more or less slow down the rotation speed of k-Imine. The large difference in irradiation light wavelength supports k-Imine as a two-way photoswitch. The photoisomerization of a-Imine obeys a similar but fully barrierless pattern while requiring a higher excitation energy to reach the (nN,π*) state. The good directionality of thermal isomerization toward E(a-Imine), plus the barrierless photoisomerization, allows for the design of a thermal and photo-operated switch. For both imines, a minimal-energy crossing point (MECI) located at the perpendicular region, with low relative energy and close to the rotary path, ensures the directionality of C═N bond rotation and confirms imines as optimal candidates for photoswitches and motors.

[A microdeletion of chromosome 9q34.11 may cause suspected cerebral palsy].

OBJECTIVE: To identify the genetic cause for a child with mental retardation and dyskinesia. METHODS: After the routine genetic counseling for the child and the core family members, conventional peripheral blood karyotyping with G-banding and tandem mass spectrometry were applied to find the common genetic problems. Array-comparative genomic hybridization (aCGH) based on the whole genome level was performed to detect minor chromosomal structural abnormalities and the result was confirmed by multiplex ligation dependent probe amplification (MLPA). RESULTS: The proband's karyotype was normal. There were not obvious abnormalities for the testing of 26 types of congenital metabolic diseases. A -2.11 Mb microdeletion of chromosome 9q34.11 region was found though aCGH, which including SPTAN1, TOR1A and other nearly 50 genes related to mental retardation, early infantile spasms, epileptic encephalopathy, myelin dysplasia and dystonia. The -2.11 Mb chromosomal microdeletion was identified by MLPA. CONCLUSION: The 2.11 Mb microdeletion of chromosome 9q34.11 region may lead to suspected cerebral palsy. Cytogenetic methods combined with MLPA and aCGH can efficiently identify genetic etiology and provide accurate results for clinical diagnosis.

Neonatal cytokines associated with infant overweight and obesity at 1 year of age.

OBJECTIVE: The incidence of childhood overweight and obesity has been increasing in recent years. Immune dysregulation has been demonstrated as a condition related to childhood obesity. Whether the neonatal immune status is related to infant overweight and obesity at 1 year of age is unclear. METHODS: To explore the relationship between neonatal cytokines and infant overweight and obesity, we conducted a prospective study in Suzhou Municipal Hospital Affiliated to Nanjing Medical University from 2015 to 2016. 514 neonates were recruited and their dried blood spots were collected after birth. Infants were grouped into normal size groups and overweight and obesity groups based on BMI at 1 year of age. 27 neonatal cytokines levels were compared between the two groups. RESULTS: 370 infants were included in final analysis. Granulocyte colony stimulating factor (GCSF), interleukin-17A (IL17A) and platelet derived growth factor-BB (PDGF-BB) levels were independently associated with childhood overweight and obesity (OR =1.27, 95%CI 1.03, 1.57; OR =1.29, 95%CI: 1.06, 1.60; OR =0.69, 95%CI: 0.49, 0.96). Additionally, neonatal GCSF and IL17A levels were positively associated with increased BMI (ß = 0.11, 95%CI: 0.02, 0.19; ß = 0.07, 95%CI 0.01, 013) and BMI z-scores (ß = 0.10, 95%CI: 0.02, 0.18; ß = 0.06, 95%CI 0.01, 0.13). Neonatal PDGF-BB levels were negatively associated with BMI (ß = -0.12, 95%CI: -0.23, -0.01) and BMI z-scores (ß = -0.12, 95%CI: -0.23, -0.01). The inverse probability weighting (IPW) was performed to account for potential selection bias of this study, and the results were consistent with the above mentioned findings. CONCLUSIONS: Neonatal GCSF, IL17A and PDGF-BB levels were correlated with infant overweight and obesity at 1 year of age, suggesting that early life immune status play a significant role of late obesity.

LncRNA DANCR restrained the survival of mycobacterium tuberculosis H37Ra by sponging miR-1301-3p/miR-5194.

Tuberculosis is a worldwide contagion caused by Mycobacterium tuberculosis (MTB). MTB is characterized by intracellular parasitism and is semi-dormant inside host cells. The persistent inflammation caused by MTB can form a granuloma in lesion regions and intensify the latency of bacteria. In recent years, several studies have proven that long non-coding RNAs (lncRNAs) play critical roles in modulating autophagy. In our study, the Gene Expression Omnibus (GEO) databases were searched for lncRNAs that are associated with tuberculosis. We found that lncRNA differentiation antagonizing non-protein coding RNA (DANCR) increased in the peripheral blood samples collected from 54 pulmonary tuberculosis patients compared to 23 healthy donors. By constructing DANCR overexpression cells, we analyzed the possible cellular function of DANCR. After analyzing our experiments, it was found that the data revealed that upregulation of DANCR facilitated the expression of signal transducer and activator of transcription 3, autophagy-related 4D cysteine peptides, autophagy-related 5, Ras homolog enriched in the brain, and microtubule-associated protein 1A/1B light chain 3 (STAT3, ATG4D, ATG5, RHEB, and LC3, respectively) by sponging miR-1301-3p and miR-5194. Immunofluorescence analysis indicated that DANCR played a positive role in both autophagosome formation and fusion of autolysosomes in macrophages. The colony-forming unit (CFU) assay data also showed that the cells overexpressing DANCR were more efficient in eliminating the intracellular H37Ra strain. Consequently, these data suggest that DANCR restrained intracellular survival of M. tuberculosis by promoting autophagy via miR-1301-3p and miR-5194.

[Application of next-generation sequencing technology for genetic diagnosis of Duchenne muscular dystrophy].

OBJECTIVE: To detect genetic causes of Duchenne muscular dystrophy (DMD). METHODS: Next-generation sequencing was used to detect 6 DMD patients in whom no exonic deletions were detected by multiplex PCR. Sanger sequencing and multiplex ligation-dependent probe amplification were used to confirm the results. RESULTS: One case was found to have deletions of exons 10 and 11, 1 had exons 16 and 17 duplication, 4 cases have 8 point mutations including c.2776C>T, c.5475delA, c.6391_6392delCA, IVS64+1G>A, c.2645A>G, c.5244G>A, c.7728T>C, c.8729A>T, c.8734A>G and c.8810G>A. The former 4 mutations are suspicious pathogenicity, the other 6 mutations are polymorphisms in population. Three novel mutations (IVS64+1G>A, c.6391_6392delCA (p.Q2131NfsX3) and p.Q926X (CAG>TAG) were not reported before. CONCLUSION: Next-generation sequencing technology is a useful tool for the detection of deletion, duplication and point mutation, which is valuable for clinical application.

[Analysis of GJB2 gene and mitochondrial DNA A1555G mutations in 16 families with non-syndromic hearing loss].

OBJECTIVE: To screen for genetic mutations in families featuring non-syndromic hearing loss. METHODS: Sixteen families with non-syndromic hearing loss were interviewed to identify medical histories by a questionnaire. Audiological and neurological examinations were conducted for all families. Coding regions of GJB2 and 12S rRNA genes were amplified and sequenced. RESULTS: Of the 17 patients with sensorineural hearing loss, 3 were homozygous mutation for GJB2 235 delC, 1 was 235 delC heterozygous mutation, 1 was 235 delC+299_300 delAT compound heterozygous mutation, and 6 were 79G>A+341G>A heterozygosis in cis mutation. No 1555A>G mutation of mitochondrial DNA (mtDNA) was found in the 16 families. CONCLUSION: The incidence of mtDNA 12S rRNA 1555A>G mutation in Jiangsu province may be lower than the average across China. Mutations of GJB2 genes may account for as much as 64.7% of non-syndromic hearing loss in this study. Screening for such mutations and genetic counseling may play an important role in the prevention of hereditary hearing loss.

[Genetic screening of mutation hot-spots for nonsyndromic hearing loss in southern Jiangsu province with SNaPshot].

OBJECTIVE: To investigate the mutation frequency in 7 mutation hot-spots of deafness gene in southern Jiangsu province and verify the performance of the SNaPshot technology platform, designed for genetic screening of non-syndromic hearing loss (NSHL) in Chinese. METHODS: One hundred and twenty-five NSHL patients were enrolled. Amplification of 235delC, 299-300delAT in GJB2 gene, IVS7-2A>G, 2168 A>G in SLC26A4 gene, and 1555A>G, 7445 A>G and 3243 A>G in mitochondrial DNA (mtDNA) was performed using multiplex polymerase chain reaction (PCR) technology. Afterwards, the sequence-specific probe interrogated each locus and labeled it at the 3' end using fluorescent dideoxynucleotide chemistry by the SNaPshot Multiplex Kit, the resulting products were then separated electrophoretically in ABI PRISM R 3130 Genetic Analyzer and analyzed in the presence of a fifth-dye-labeled size standard. Finally, the genotyping results were verified by direct sequencing or PCR-restriction fragment length polymorphism (PCR-RFLP). RESULTS: (1) The total mutation frequency for the 7 mutation hot-spots was 53.6%. The mutation frequency of 235delC was 24.0%, 299-300delAT was 5.6% in the GJB2 gene, IVS7-2A>G was 15.2%, 2168A>G was 3.2% in the SLC26A4 gene. The mutation frequency of 1555A>G and 7445 A>G in mtDNA was 4.8% and 0.8% respectively. The mutation 3243 A>G was not detected. (2) The SNaPshot results were consistent with that from direct sequencing or PCR-RFLP, and the specificity and sensitivity of detection were 100%. CONCLUSION: (1) More than half of the patients with deafness in southern Jiangsu province carry the mutations of the seven hot-spots. (2) The genetic screening technology platform based on SNaPshot can detect 7 mutations in one reaction, and is efficient and suitable for clinical practice.

Whole-exome sequencing identified a novel mutation in CHM of a Chinese family.

Choroideraemia (CHM) is a rare X-linked progressive-inherited retinal disease. In this study, we diagnosed and explored the genetic cause in a Chinese pedigree exhibiting nyctalopia and decreased visual acuity in early life. Clinical data and peripheral blood samples were collected from available family members. Sanger sequencing of RPGR and RP2 genes, and subsequently whole-exome sequencing was carried out to investigate the molecular cause. The proband was initially diagnosed as retinitis pigmentosa and experienced night blindness at an early age and decreased visual acuity in teens. The other affected males in this family suffered from the same problem. Direct sequencing failed to reveal the genetic cause and hence a novel hemizygous mutation c.861_862insGCTT was detected by WES in CHM gene resulting in a premature stop codon and a truncated protein. Subsequently, it was confirmed by Sanger sequencing and cosegregation analysis. We describe a novel mutation c.861_862insGCTT in CHM gene in a Chinese pedigree with choroideraemia. Our study emphasizes the utilization of next-generation sequencing in the diagnosis and genetic analysis of retinal diseases.

Gut Microbiota Exceeds Cervical Microbiota for Early Diagnosis of Endometriosis.

The diagnosis of endometriosis is typically delayed by years for the unexclusive symptom and the traumatic diagnostic method. Several studies have demonstrated that gut microbiota and cervical mucus potentially can be used as auxiliary diagnostic biomarkers. However, none of the previous studies has compared the robustness of endometriosis classifiers based on microbiota of different body sites or demonstrated the correlation among microbiota of gut, cervical mucus, and peritoneal fluid of endometriosis, searching for alternative diagnostic approaches. Herein, we enrolled 41 women (control, n = 20; endometriosis, n = 21) and collected 122 well-matched samples, derived from feces, cervical mucus, and peritoneal fluid, to explore the nature of microbiome of endometriosis patients. Our results indicated that microbial composition is remarkably distinguished between three body sites, with 19 overlapped taxa. Moreover, endometriosis patients harbor distinct microbial communities versus control group especially in feces and peritoneal fluid, with increased abundance of pathogens in peritoneal fluid and depletion of protective microbes in feces. Particularly, genera of Ruminococcus and Pseudomonas were identified as potential biomarkers in gut and peritoneal fluid, respectively. Furthermore, novel endometriosis classifiers were constructed based on taxa selected by a robust machine learning method. These results demonstrated that gut microbiota exceeds cervical microbiota in diagnosing endometriosis. Collectively, this study reveals important insights into the microbial profiling in different body sites of endometriosis, which warrant future exploration into the role of microbiota in endometriosis and highlighted values on gut microbiota in early diagnosis of endometriosis.

[22q11 microdeletion test in patients with congenital heart defects by quantitative fluorescent PCR].

OBJECTIVE: To establish an assay for screening chromosome 22q11 microdeletion efficiently, and apply it for detecting del22q11 in patients with non-syndromic congenital heart defects (CHD). METHODS: Seventy nine patients with non-syndromic CHD and 84 normal controls were genotyped for 8 short tandem repeat (STR) markers located in 22q11 region, by using quantitative fluorescence polymerase chain reaction (QF-PCR). RESULTS: The average heterozygosity of the STR markers in patients and controls was 0.76 and 0.79, respectively. One patient with Tetralogy of Fallot (TOF) from the 79 CHD cases (1.3%) was found to have a deletion within chromosome 22q11.2, which was confirmed by multiplex ligation-dependent probe amplification (MLPA). CONCLUSION: The QF-PCR assay developed in this study was a reliable and an efficient alterative approach to screen for 22q11 microdeletion in clinical diagnosis and genetic counseling.

Two heterozygous mutations in the ERCC6 gene associated with Cockayne syndrome in a Chinese patient.

OBJECTIVE: To confirm diagnosis and explore the genetic aetiology in a Chinese patient suspected to have Cockayne syndrome (CS). METHODS: The patient was clinically examined, and the patient and her biological parents underwent genetic analysis using whole exome sequencing (WES) and Sanger sequencing. The foetus of the patient's mother underwent prenatal diagnostic Sanger sequencing using amniotic fluid obtained at 19 weeks' gestation. RESULTS: Clinical examination of the patient showed developmental delay, progressive neurologic dysfunction and premature aging. Two compound, heterozygous ERCC excision repair 6, chromatin remodelling factor (ERCC6) gene mutations were detected in the proband by WES and confirmed by Sanger sequencing, comprising a known paternal nonsense mutation (c.643G > T, p.E215X) and a novel maternal short insertion and deletion mutation (c.1614_c.1616delGACinsAAACGTCTT, p.K538_T539delinsKNVF). The patient was consequently diagnosed with CS type I. The foetus of the patient's mother was found to carry only the maternally-derived c.1614_c.1616delGACinsAAACGTCTT variant. CONCLUSION: This study emphasized the value of WES in clinical diagnosis, and enriched the known spectrum of ERCC6 gene mutations.

Clinical Utility of SNP Array Analysis in Prenatal Diagnosis: A Cohort Study of 5000 Pregnancies.

BACKGROUND: Single nucleotide polymorphism array (SNP-array) has been introduced for prenatal diagnosis. We aimed to evaluate the clinical value of SNP-array in the diagnosis of fetal chromosomal anomalies. METHODS: A retrospective study was conducted on 5000 cases tested by SNP-array, and the results of 4022 cases analyzed by both karyotyping and SNP-array were compared. RESULTS: SNP-array analysis of 5000 samples revealed that the overall abnormality detection rate by SNP-array was 12.3%, and the overall detection rate of clinically significant copy number variations (CNVs) by SNP-array was 2.6%. SNP-array identified clinically significant submicroscopic CNVs in 4.5% fetuses with anomaly on ultrasonography, in 1.6% of fetuses with advanced maternal age (AMA), in 2.5% of fetuses with abnormal result on maternal serum screening, in 2.9% of fetuses with abnormal non-invasive prenatal testing (NIPT) results and in 3.0% of fetuses with other indications. Of the 4022 samples analyzed by both karyotyping and SNP-array, SNP-array could identify all the aneuploidy and triploidy detected by karyotyping but did not identify balanced structural chromosomal abnormalities and low-level mosaicism detected by karyotyping. CONCLUSION: SNP-array could additionally identify clinically significant submicroscopic CNVs, and we recommend the combination of SNP-array analysis and karyotyping in prenatal diagnosis.

Correction to: miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.

An amendment to this paper has been published and can be accessed via the original article.

[Research on the illuminance characteristics of LED surguical luminaire].

The illuminance characteristics of LED (Lighting Emitting Diode) Surgical Luminaire is researched in this paper from the aspects of the LED Single-tube illumination analysis, LED arrays distribution and lighting design. The facula distribution characteristics of the LED prototype and multi-facet entirety reflection Surgical Luminaire is tested and compared according to the standards. The results of experimental show that LED prototype can fully meet the surgical illumination requirements, and the LED's own characteristics and further development will greatly broaden the space of medical lighting.

Experimental factors are associated with fetal fraction in size selection noninvasive prenatal testing.

Every year, 4-6 million pregnant women undergo noninvasive prenatal testing (NIPT), which is used worldwide for fetal aneuploidy screening. Adequate fetal cell-free DNA (cfDNA) is the critically important factor to ensure high sensitivity and specificity. In this study, we sought to increase the fetal fraction by adjusting experimental factors in the size selection for NIPT. CfDNA was extracted from 1495 pregnant women at 12-26 weeks of gestation for sequencing of shorter cfDNA NIPT (< 140 bp). Multivariable linear regression models were used to evaluate the association between experimental factors and fetal fraction. Nomograms for the likelihood of high fetal fraction (> 20%) were constructed according to significant factors in multivariable regression models. Our results suggested that cfDNA and library concentrations were negatively correlated with fetal fraction, and uniquely mapped reads were positively correlated with fetal fraction. Lower cfDNA and library concentrations, shorter cfDNA fragments, and higher uniquely mapped reads may be more conducive to obtaining higher fetal fractions. Furthermore, we constructed easy-to-use nomograms incorporating the maternal, fetal characteristics and experimental factors to precisely predict the probability of high fetal fraction with an area under the curve (AUC) of 0.773 (95% confidence interval: 0.749-0.797). Collectively, our maternal plasma cfDNA-based nomograms consider experimental factors that can be adjusted and may improve a laboratory's ability to obtain higher fetal cfDNA concentrations.

The long intergenic non-protein coding RNA 707 promotes proliferation and metastasis of gastric cancer by interacting with mRNA stabilizing protein HuR.

Multiple studies have revealed that long non-coding RNAs (lncRNAs) extensively participate in human cancer malignant progression. The long intergenic non-protein coding RNA 707 (LINC00707), 3087 bp in length, was recently reported to be an essential oncogene in promoting lung adenocarcinoma cell proliferation and metastasis. However, its role in gastric cancer (GC) remains unclear. In this study, we identified that LINC00707 was excessively expressed in GC tissues and correlated with advanced stage, larger tumor size, lymph node metastasis and poorer prognosis in GC patients. In vitro and in vivo assays showed that LINC00707 promote GC cell proliferation and metastasis. Mechanistically, LINC00707 could abundantly interact with mRNA stabilizing protein HuR; "LINC00707-HuR" coalition ulteriorly combined with VAV3/F11R mRNAs and increased their stability. Taken together, our findings prove that LINC00707 may act as an oncogene in GC by regulating mRNA stability and serve as a potential target for GC diagnosis and prognosis.