Lifestyle factors, physical health, and life satisfaction under different changes in depressive symptoms among Chinese community-dwelling older adults: A longitudinal analysis.

BACKGROUND: The study aims to investigate the long-term impact of lifestyle-related factors and physical health on life satisfaction and depressive symptoms among Chinese community-dwelling older adults. METHODS: Using data from the China Health and Retirement Longitudinal Study (CHARLS), the analytic sample of this study included 1,068 older adults who had participated in the surveys in both 2011 and 2018. Multivariate regression was employed to analyze both cross-sectional and longitudinal relationships between lifestyle-related factors, physical health, and subjective well-being - specifically depressive symptoms and life satisfaction. Additionally, the model tested how these factors correlate with life satisfaction across different groups of depressive symptom changes among older adults, categorized as not at risk of depression, intermittent depression, and chronic depression. RESULTS: Multimorbidity was significantly related to baseline and follow-up depressive risk in older adults. Shorter sleep duration was associated with baseline depression risk. Current alcohol drinkers reported significantly more severe depressive symptoms than non-drinkers. At baseline, current smokers were more likely to have a lower degree of life satisfaction than nonsmokers. Among older adults with chronic depression at the 7-year follow-up, former smokers tended to have lower life satisfaction than nonsmokers. CONCLUSIONS: Our findings identified drinking alcohol and having a shorter sleep duration as modifiable lifestyle-related risk factors for late-life depression and smoking as a detrimental factor for life satisfaction in older Chinese adults. Multimorbidity was a significant predictor of more depressive symptoms. Our findings have implications for future psychosocial interventions that target the alleviation of depressive symptoms and the promotion of life satisfaction in older Chinese people based on their different long-term mental and physical health conditions.

Dyadobacter diqingensis sp. nov., isolated from Baima snow mountain of Diqing Tibetan Autonomous Prefecture in Yunnan province, south-west China.

A Gram-negative, aerobic, nonmotile, rod-shaped and yellow-pigment-producing bacteria was isolated from Baima snow mountain of Diqing Tibetan Autonomous Prefecture in Yunnan province, south-west China and characterized using a polyphasic approach. The results of 16S rRNA gene sequence similarity analysis showed that strain YIM B04101T was closely related to the type strain of Dyadobacter koreensis DSM 19938T (97.81%) and Dyadobacter frigoris AR-3-8T (97.95%). The predominant respiratory quinone was menaquinone-7 (MK-7). The major polar lipid was phosphatidylethanolamine. The major fatty acids were summed feature 3 (C16:1ω7c/C16:1ω6c), C18:1ω9c and C16:0. The DNA G + C content was 43.5 mol%. Phylogenetic analysis based on 16S rRNA gene sequences indicated that the strain YIM B04101T belonged to a cluster comprising species of the genus Dyadobacter. However, it differed from its closest relative, Dyadobacter koreensis KCTC 12537T and Dyadobacter frigoris AR-3-8T, in many physiological properties. Based on these phenotypic characteristics and phylogenetic distinctiveness, strain YIM B04101T is considered to be a novel species of the genus Dyadobacter, for which the name Dyadobacter diqingensis sp. nov. is proposed. The type strain is YIM B04101T (= CGMCC 1.19249T = CCTCC AB 2021270).

Caldalkalibacillus salinus sp. nov., isolated from a salt lake in Xinjiang, northwest China.

A novel Gram-stain-negative, aerobic, motile and rod-shaped bacterium, designated as strain YIM B00319T, was isolated from a sediment sample obtained from Wuzunbulake salt Lake in Xinjiang Uygur Autonomous Region, northwest China. Phylogenetic analysis based on 16S rRNA gene sequences along with the whole genome showed that strain YIM B00319T belongs to the family Bacillaceae and was most closely related to Bacillus horti K13T and Caldalkalibacillus mannanilyticus JCM 10596T, with sequence similarities of 95.7% and 94.6%, respectively. The genome of strain YIM B00319T was 3.77 Mbp with a DNA G + C content of 43%. Strain YIM B00319T grew at 15-45 ℃, pH 7.0-9.5 and with 3-11% (w/v) NaCl. The major respiratory quinone of strain YIM B00319T was MK-7, and the major fatty acids (> 10%) were iso-C15:0, anteiso-C15:0, and summed feature 3 (C16:1 ω6c and/or C16:1 ω7c). The main polar lipids were phosphatidylethanolamine (PE), phosphatidylglycerol (PG), and diphosphatidylglycerol (DPG). The cell-wall peptidoglycan contained meso-diaminopimelic acid. On the basis of the phenotypic, chemotaxonomic, genomic, and phylogenetic information, strain YIM B00319T represents a novel species of the genus Caldalkalibacillus, for which the name Caldalkalibacillus salinus sp. nov. is proposed. The type strain is YIM B00319T (= CGMCC 1.18750T = NBRC 115338T).

POTEE promotes colorectal carcinoma progression via activating the Rac1/Cdc42 pathway.

Current studies have shown that POTE ankyrin domain family members have high expressions as tumor antigens in malignant tumors, such as prostate cancer, ovarian cancer, breast cancer and the like. POTEE is a member of the POTE anchor protein family E. However, its role in colorectal carcinoma (CRC) has not been studied. In this study, the function of POTEE in CRC was examined for the first time and its correlation with CRC cell biological behaviors was analyzed. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry revealed that POTEE was remarkably overexpressed in CRC and associated with an aggressive phenotype. We also found that POTEE was localized in the cytoplasm. In addition, downregulation of POTEE expression can notably inhibit the proliferation, migration, and invasion of CRC cell in vitro, and repressed tumor growth and metastasis in vivo. In contrast, overexpression of POTEE could promote the aggressive behaviors of CRC cells. Mechanistically, POTEE promoted CRC migration, invasion and epithelial-mesenchymal transition (EMT) by increasing the activation of Rac1 and Cdc42. To summarize, these results suggested that POTEE might serve as an oncogene for CRC tumorigenesis and progression, and may become a novel molecular marker for clinical diagnosis and treatment.

[Corrigendum] Knockdown of lncRNA HNF1A-AS1 inhibits oncogenic phenotypes in colorectal carcinoma.

Following the publication of the article, the authors noted an error associated with the presentation of Fig. 3B. This Figure part showed the cell cycle analysis as determined by flow cytometry of HT29 cells transfected with either a HNF1A-AS1-specific siRNA or a negative control siRNA at 48 h post-transfection. An error was made in the compilation of this Figure, and the same data were inadvertently selected to represent the cell cycle analysis of both the HT29-SI and the HT29-NC cells (i.e., the data relating to the HT29-NC cells were included in the Figure twice). A corrected version of Fig. 3 is shown on the next page. Note that this correction affects neither the interpretation of the data nor the reported conclusions of this work. The authors all agree to this Corrigendum, and regret that this error went unnoticed during the proofs correction stage. They also wish to thank the Editor for allowing them the opportunity to publish this Corrigendum, and regret any inconvenience this error has caused. [the original article was published in Molecular Medicine Reports 16: 4694-4700, 2017; DOI: 10.3892/mmr.2017.7175].

MIER3 suppresses colorectal cancer progression by down-regulating Sp1, inhibiting epithelial-mesenchymal transition.

Mesoderm induction early response 1, family member 3 (MIER3) has recently been identified as a potential cancer susceptibility gene. However, the expression pattern and the role of MIER3 in the progression of colorectal cancer (CRC) have not yet been well characterized. Here, we reported that MIER3 was significantly reduced in human primary colorectal cancer and was associated with CRC metastasis and poor prognosis. Moreover, the up-regulation of MIER3 expression significantly inhibited CRC cell proliferation, migration and invasion in vitro and repressed tumor growth and metastasis in vivo. In contrast, down-regulation of MIER3 could promote the aggressive behaviors of CRC cells. Furthermore, our study showed that MIER3 inhibited cell proliferation and invasion partially via reduction of Sp1 and subsequent suppression of epithelial-mesenchymal transition (EMT). In conclusion, our data suggested that MIER3 plays a potential tumor suppressor role in CRC progression and may be a potentially valuable clinical prognostic marker of this disease.

Knockdown of lncRNA HNF1A-AS1 inhibits oncogenic phenotypes in colorectal carcinoma.

Long non-coding RNAs (lncRNAs) have been demonstrated to serve important roles in the development and progression of cancer. Recently HNF1A antisense RNA 1 (HNF1A­AS1), a lncRNA, has been reported as exhibiting a potential oncogenic role in the development of many types of cancer. However, the expression and the role of HNF1A­AS1 in colorectal carcinoma (CRC) remains unclear. In the present study, the role of HNF1A­AS1 in CRC was examined for the first time and its correlation with CRC cell biological behaviors was analyzed. The results demonstrated that HNF1A­AS1 was distinctly upregulated in CRC tissues and associated with CRC metastasis to the lymph nodes. Reverse transcription­quantitative polymerase chain reaction revealed that HNF1A­AS1 was also upregulated in CRC cell lines and localized in the nucleus. In addition, knockdown of HNF1A­AS1 expression notably inhibited CRC cell proliferation, migration, invasion and colony formation, and suppressed S­phase entry in vitro. Taken together, these results suggested that HNF1A­AS1 might serve as a promising prognostic marker for CRC tumorigenesis and progression.

[Expression of MIER3 in colorectal cancer and bioinformatic analysis of MIER3- interacting proteins].

OBJECTIVE: To explore role of MIER3 gene in the development and progression of human colorectal carcinoma (CRC) and analyze the proteins that interact with MIER3 using bioinformatic techniques. METHODS: MIER3 mRNA and protein expressions were detected in 8 CRC biopsy samples and paired adjacent tissues using real-time PCR and Western blotting. A recombinant eukaryotic expression vector pcDNA3-MIER3 was constructed and its effect on the proliferation and invasion of CRC cells were tested using CCK8 assay and Transwell migration assay. Bioinformatic methods were used to predict and analyze MIER3-interacting proteins. RESULTS: MIER3 was obviously down-regulated in the 8 CRC tissues as compared with the paired adjacent tissues. In human CRC cell line DLD1, MIER3 overexpression induced by transfection of the cells with pcDNA3-MIER3 significantly inhibited the cell proliferation and suppressed cell invasiveness in vitro. Bioinformatics analyses indicated that NAT9 was a potential MIER3-interacting protein and MIER3 was probably associated with tumor susceptibility. CONCLUSION: MIER3, which is obviously down-regulated in CRC tissues, is closely associated with the proliferation and invasion of CRC, and NAT9 protein is a probable MIER3-interacting protein.

Long non-coding RNA FEZF1-AS1 facilitates cell proliferation and migration in colorectal carcinoma.

Long non-coding RNAs (lncRNA) have been shown to play important roles in the development and progression of cancer. Here, we discovered a novel long noncoding RNA (lncRNA) FEZF1 antisense RNA1 (FEZF1-AS1) is markedly upregulated in human primary colorectal carcinoma (CRC) and associated with CRC metastasis and poor prognosis. Moreover, the downregulation of FEZF1-AS1 expression significantly inhibited the CRC cells proliferation, migration and invasiveness, suppressed S-phase entry in vitro, and repressed tumor growth and metastasis in vivo. In contrast, overexpression of FEZF1-AS1 could promote the aggressive behaviors of CRC cells. We further discovered that the downregulation of FEZF1-AS1 reduced its sense-cognate gene FEZF1 mRNA and protein expression in CRC cells. There was a positive correlation between FEZF1-AS1 and FEZF1 expression in CRC. Moreover, FEZF1 knockdown also significantly suppressed CRC cell proliferation, migration, and invasion. Our findings indicate that the dysregulation of FEZF1-AS1 participates in colorectal tumorigenesis and progression, which might be achieved, at least in part, through FEZF1 induction.

[Construction of a eukaryotic expression vector of TM4SF1 and its effect on migration and invasion of colorectal cancer cells].

OBJECTIVE: To construct a eukaryotic expression vector of transmembrane-4-L-six-family-1 (TM4SF1) gene and study its effect on the migration and invasion of colorectal cancer cells. METHODS: A pair of specific primers of TM4SF1 gene (GenBank: BC034145.1) was used to acquire the open reading frame of TM4SF1 by RT-PCR. The amplified sequence was ligated to a PEZ-M29 vector, which, after identification, was transiently transfected in colorectal cancer cell lines HCT116 and DLD1. Western blotting and immunocytochemistry were used to analyze the transfection efficiency, and scratch and Transwell tests were performed to analyze the changes in the migration and invasion of HCT116 and DLD1 cells after transfection. RESULTS: Cell scratch and Transwell assays revealed that transfection with the recombinant plasmid, PEZ-M29/TM4SF1, caused up-regulated expression of TM4SF1 and promoted the migration and invasion of HCT116 and DLD1 cells. CONCLUSION: Our results demonstrated that TM4SF1 is closely related to the invasion and metastasis of colorectal cancer cells in vitro.