• D2
• Dissection
• Gastric cancer
• Lymph node
• Lymphadenectomy
• Technique

• Humans
• Stomach Neoplasms/surgery
• Stomach Neoplasms/pathology
• Lymph Node Excision/methods
• Gastrectomy/methods
• Lymph Nodes/pathology
• Lymph Nodes/surgery
• Indocyanine Green
• Prognosis

• C118P
• RAB1A
• gastric cancer
• mTOR
• protein degradation

• No.82304541 National Natural Science Foundation of China
• No.82272668 National Natural Science Foundation of China
• No.BK20221036 Natural Science Foundation of Jiangsu Province

• Breast cancer
• Drug resistance
• Epigenetic regulation
• Epigenetic therapy
• Immune cells
• Tumor microenvironment

• Humans
• Tumor Microenvironment/genetics
• Epigenesis, Genetic
• Female
• Breast Neoplasms/genetics
• Breast Neoplasms/pathology
• Breast Neoplasms/drug therapy
• Disease Progression
• Animals
• DNA Methylation/genetics
• Gene Expression Regulation, Neoplastic
• Drug Resistance, Neoplasm/genetics

• Dienogest
• MicroRNA
• Ovarian endometriosis
• Ovarian reserve

• Female
• Humans
• MicroRNAs/genetics
• Endometriosis/surgery
• Ovarian Reserve
• Cystectomy
• Biomarkers
• Anti-Mullerian Hormone

• Baicalin
• CDK16
• Cell Cycle
• Colon Cancer
• Proliferation
• miR-139-3p

• breast cancer
• development
• mammary gland
• microRNA

Detrimental exposures in mothers are recognized as risk factors for the development of metabolic dysfunction in offspring. In contrast, maternal exercise has been reported to be an effective strategy to maintain offspring health. However, the mechanisms underlying the protective effects of maternal exercise on adult offspring metabolic homeostasis are largely unclear. This study aims to investigate whether maternal exercise before and during pregnancy could combat the adverse effects of maternal high-fat diet (HFD) on metabolism in 24-week-old male offspring and to explore the role of miRNAs in mediating the effects. Female C57BL/6 mice were fed with either control diet or HFD 3-week prior to breeding and throughout pregnancy and lactation, among whom half of the HFD-fed mice were submitted to voluntary wheel running training 3-week before and during pregnancy. Male offspring were sedentary and fed with a control diet from weaning to 24 weeks. Body weight, the content of inguinal subcutaneous adipose tissue and perirenal visceral adipose tissue, glucose tolerance, and serum insulin and lipids in offspring were analyzed. Hepatic tissues were collected for transcriptome and miRNA sequencing and reverse transcription-quantitative polymerase chain reaction validation. The results showed that maternal HFD resulted in significant glucose intolerance, insulin resistance, and dyslipidemia in adult offspring, which were negated by maternal exercise. Transcriptome sequencing showed that maternal exercise reversed perinatal HFD-regulated genes in adult offspring, which were enriched in glucose and lipid metabolic-related signaling pathways. At the same time, maternal exercise significantly rescued the changes in the expression levels of 3 hepatic miRNAs in adult offspring, and their target genes were involved in the regulation of cholesterol biosynthesis and epigenetic modification, which may play an important role in mediating the intergenerational metabolic regulation of exercise. Overall, our research pioneered the role of miRNAs in mediating the programming effects of maternal exercise on adult offspring metabolism, which might provide novel insight into the prevention and treatment of metabolic disorders in early life.

miR-139-3p exerts tumor-suppressing functions in various cancers. We analyzed and identified that miR-139-3p expression was notably low in gastric cancer (GC) via edgeR differential analysis based on The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction (qRT-PCR) assay. The binding relationship between Kinesin Family Member 18B (KIF18B) and miR-139-3p was predicted by bioinformatics databases, and verified through dual-luciferase assay. Western blot and qRT-PCR results also indicated that miR-139-3p restrained KIF18 expression at mRNA and protein levels. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, transwell, flow cytometry assays were introduced to evaluate cell proliferation, migration, invasion, and cell cycle, respectively, where the results indicated that upregulating miR-139-3p inhibited proliferative, migratory, and invasive abilities of GC cells, while caused cell-cycle arrest. Moreover, the results of rescue experiments illustrated that miR-139-3p hampered the progression of GC cells by targeting and suppressing KIF18B. To sum up, we concluded that miR-139-3p suppressed GC progression by targeting KIF18B.

• Gastric cancer
• KIF18B
• invasion
• miR-139-3p
• migration
• proliferation

• HCC
• UCK2
• hepatocellular carcinoma
• invasion
• miR-139-3p
• migration
• proliferation

• cutaneous tissues
• environmental risk factors
• microRNAs
• ozone exposure

• IG2017-20699 Italian Association for Cancer Research

• Cervical cancer
• S100A14
• circ_0003221
• miR-139-3p

• Animals
• Calcium-Binding Proteins/metabolism
• Cell Proliferation/genetics
• Down-Regulation
• Female
• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Neovascularization, Pathologic/genetics
• RNA, Circular/genetics
• Uterine Cervical Neoplasms/genetics

• biomarker
• diagnosis
• endometriosis
• miRNAs

• Biomarkers/blood
• Endometriosis/blood
• Endometriosis/metabolism
• Female
• Humans
• MicroRNAs/blood

• CIHR 142230 CIHR
• Canadian Institutes of Health Research

We newly generated an RNA-sequencing-based microRNA (miRNA) expression signature of head and neck squamous cell carcinoma (HNSCC). Analysis of the signature revealed that both strands of some miRNAs, including miR-139-5p (the guide strand) and miR-139-3p (the passenger strand) of miR-139, were downregulated in HNSCC tissues. Analysis of The Cancer Genome Atlas confirmed the low expression levels of miR-139 in HNSCC. Ectopic expression of these miRNAs attenuated the characteristics of cancer cell aggressiveness (e.g., cell proliferation, migration, and invasion). Our in silico analyses revealed a total of 28 putative targets regulated by pre-miR-139 (miR-139-5p and miR-139-3p) in HNSCC cells. Of these, the GNA12 (guanine nucleotide-binding protein subunit alpha-12) and OLR1 (oxidized low-density lipoprotein receptor 1) expression levels were identified as independent factors that predicted patient survival according to multivariate Cox regression analyses (p = 0.0018 and p = 0.0104, respectively). Direct regulation of GNA12 and OLR1 by miR-139-3p in HNSCC cells was confirmed through luciferase reporter assays. Moreover, overexpression of GNA12 and OLR1 was detected in clinical specimens of HNSCC through immunostaining. The involvement of miR-139-3p (the passenger strand) in the oncogenesis of HNSCC is a new concept in cancer biology. Our miRNA-based strategy will increase knowledge on the molecular pathogenesis of HNSCC.

• GNA12
• HNSCC
• OLR1
• expression signature
• miR-139-3p
• miR-139-5p
• microRNA
• passenger strand
• tumor suppressor

The validity of lymphadenectomy of the lymph node along the superior mesenteric vein (LN14v) in gastric cancer remains controversial. The study investigated the characteristics and prognosis of gastric cancer with metastasis or micrometastasis to LN14v.

A retrospective study of 626 patients undergoing radical gastrectomy in our center from January 2003 to December 2015 was analyzed. In total, 303 patients had lymphadenectomy of LN14v, and lymph node micrometastasis was evaluated by immunohistochemical staining for cytokeratin nodes CK8/18. A logistic regression model was applied to confirm the predictive factors of micrometastasis. Survival analysis was performed to evaluate the effect of micrometastasis or metastasis on prognosis.

The metastatic rate of the LN14v lymph node was 15.8%, and the micrometastatic rate was 3.3%. Multivariate analysis showed site, Borrmann classification, postoperative lymph node metastasis (pN), and metastasis in LN6 and LN9 were predictive factors for LN14v micrometastasis or metastasis (P < 0.05). The 5-year survival rate in the positive group (LN14v micrometastasis or metastasis) was 12.4%. The prognosis of patients without LN14v lymph node micrometastasis was better than that of the positive group, whereas the difference between group of LN14v micrometastasis and LN14v metastasis was not obvious. In matched analysis, patients with stage III gastric cancer L/M area, pN2-3, and LN6(+) who underwent lymphadenectomy of LN14v had better survival than those without lymphadenectomy of LN14v.

Lymph node micrometastasis may provide accurate prognostic information for patients with gastric cancer. Moreover, lymphadenectomy of LN14v might improve the survival of patients with stage III gastric cancer of L/M area, pN2-3, and LN6(+).

• gastric carcinoma (GC)
• immunohistochemistry (IHC)
• metastasis to the lymph node
• micrometastases
• prognosis

Breast cancer is a complex, heterogeneous disease at the phenotypic and molecular level. In particular, the transcriptional regulatory programs are known to be significantly affected and such transcriptional alterations are able to capture some of the heterogeneity of the disease, leading to the emergence of breast cancer molecular subtypes. Recently, it has been found that network biology approaches to decipher such abnormal gene regulation programs, for instance by means of gene co-expression networks, have been able to recapitulate the differences between breast cancer subtypes providing elements to further understand their functional origins and consequences. Network biology approaches may be extended to include other co-expression patterns, like those found between genes and non-coding transcripts such as microRNAs (miRs). As is known, miRs play relevant roles in the establishment of normal and anomalous transcription processes. Commodore miRs (cdre-miRs) have been defined as miRs that, based on their connectivity and redundancy in co-expression networks, are potential control elements of biological functions. In this work, we reconstructed miR–gene co-expression networks for each breast cancer molecular subtype, from high throughput data in 424 samples from the Cancer Genome Atlas consortium. We identified cdre-miRs in three out of four molecular subtypes. We found that in each subtype, each cdre-miR was linked to a different set of associated genes, as well as a different set of associated biological functions. We used a systematic literature validation strategy, and identified that the associated biological functions to these cdre-miRs are hallmarks of cancer such as angiogenesis, cell adhesion, cell cycle and regulation of apoptosis. The relevance of such cdre-miRs as actionable molecular targets in breast cancer is still to be determined from functional studies.

• biological networks
• computational oncology
• hallmarks of cancer
• micro-RNA
• multi-omics

Bone metastases cause substantial morbidity and implicate worse clinical outcomes for clear-cell renal cell carcinoma patients. MicroRNAs are small RNA molecules that modulate gene translation and are involved in the development of cancer and metastasis. We identified six microRNAs that are potentially specifically involved in metastasis to bone, of which two seem protective and four implicate a higher risk. This aids further understanding of the process of metastasizing to bone. Furthermore, these microRNA hold potential for biomarkers or therapeutic targets.

Bone metastasis in clear-cell renal cell carcinoma (ccRCC) leads to substantial morbidity through skeletal related adverse events and implicates worse clinical outcomes. MicroRNAs (miRNA) are small non-protein coding RNA molecules with important regulatory functions in cancer development and metastasis. In this retrospective analysis we present dysregulated miRNA in ccRCC, which are associated with bone metastasis. In particular, miR-23a-3p, miR-27a-3p, miR-20a-5p, and miR-335-3p specifically correlated with the earlier appearance of bone metastasis, compared to metastasis in other organs. In contrast, miR-30b-3p and miR-139-3p were correlated with less occurrence of bone metastasis. These miRNAs are potential biomarkers and attractive targets for miRNA inhibitors or mimics, which could lead to novel therapeutic possibilities for bone targeted treatment in metastatic ccRCC.

• SATB2
• bone metastasis
• miR-139-3p
• miR-20a-5p
• miR-23a-3p
• miR-27a-3p
• miR-30b-3p
• miR-335-3p
• microRNA
• renal cell carcinoma

LncRNA MEG3 expressed abnormally in various cancers including breast cancer, but no studies reported the correlation between MEG3 SNPs and breast cancer susceptibility among Chinese women.

This study is aimed to explore the association between three SNPs of MEG3 (rs3087918, rs7158663, rs11160608) and breast cancer. The study is a population-based case-control study including 434 breast cancer patients and 700 healthy controls. Genotyping was performed using Sequenom MassArray technique. Function prediction of rs3087918 were based on RNAfold and lncRNASNP2 databases.

Pooled analysis indicated that rs3087918 was related to a decreased risk of breast cancer [GG vs. TT: OR (95%) = 0.67(0.45–0.99), P = 0.042; GG vs. TT + TG: OR (95%) = 0.69(0.48–0.99), P = 0.046], especially for women aged <=49 [GG vs. TT: OR (95%) = 0.40(0.22–0.73), P = 0.02]. Comparison between case groups showed genotype GG and TG/GG of rs3087918 were associated with her-2 receptor expression [GG vs. TT: OR (95%) = 2.37(1.24–4.63), P = 0.010; TG + GG vs. TT: OR (95%) = 1.50(1.01–2.24), P = 0.045]. We didn’t find statistical significance for rs11160608, rs7158663 and breast cancer. Structure prediction based on RNAfold found rs3087918 may influence the secondary structure of MEG3. The results based on lncRNASNP2 indicated that rs3087918 may gain the targets of hsa-miR-1203 to MEG3, while loss the target of hsa-miR-139-3p and hsa-miR-5091 to MEG3.

MEG3 rs3087918 was associated with a decreased risk of breast cancer. MEG3 haplotype TCG may increase the risk of breast cancer.

• Breast cancer
• Case-control study
• MEG3
• SNP
• miRNA

• breast cancer
• cell line
• miRNA-based therapeutics
• microRNAs

• 5535000 Trans-disciplinary Research Grant Scheme

• Laryngeal cancer
• Smad3
• circ_0000218
• microRNA-139-3p

• Biomarkers
• Gastrectomy
• Gastric cancer
• Lymphadenectomy
• Minimally invasive surgery
• Molecular classification

• AAA
• GRIA4
• LYPD3
• VSMC apoptosis
• circCBFB
• miR-28-5p

Radical gastrectomy with D2 lymph node (LN) dissection is the standard surgical procedure for patients with resectable gastric cancer (GC). In the fifteenth edition of the Japanese Classification of Gastric Carcinoma, the 14v LN (LNs along the root of the superior mesenteric vein) was defined as the regional gastric LN. The efficacy of 14v LN dissection during radical distal gastrectomy for lower-third GC remains controversial.

To analyze whether the addition of 14v LN dissection improved the survival of patients with lower-third GC.

The data from 65 patients who underwent 14v LN dissection and 65 patients treated without 14v LN dissection were selected using the propensity score-matched method from our institute database constructed between 2000 and 2012. Overall survival was compared between the groups.

Overall survival was similar between patients with 14v LN metastasis and those with distant metastasis (P = 0.521). Among patients with pathological stage IIIA disease, those who were treated with 14v LN dissection had a significantly higher overall survival than those treated without it (P = 0.020). Multivariate analysis showed that age < 65 years and pT2-3 stage were independent favorable prognostic factors for prolonged overall survival in patients with pathological stage IIIA disease. Patients with No. 1, No. 6, No. 8a, or No. 11p LN metastasis were at higher risk of having 14v LN metastasis.

Adding 14v LN dissection to D2 dissection during radical distal gastrectomy may improve the overall survival of patients with pathological stage IIIA lower-third GC.

• Gastric cancer
• No. 14v lymph node
• Lymphadenectomy
• Prognosis
• Propensity score matching