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1.
Front Public Health ; 11: 1303541, 2023.
Article in English | MEDLINE | ID: mdl-38074713

ABSTRACT

The primary prerequisite for socioeconomic growth is good health, hence promoting residents' health is a vital objective of public policies. It is yet up for debate whether or not the digital economy (DE), which will be crucial to future economic growth, will eventually result in improvements in residents' health. Utilizing the China Family Panel Studies (CFPS) data in 2020, we explore how the DE affects residents' health. The findings reveal that residents' health is greatly enhanced by the DE. The eastern region sees a more dramatic improvement in residents' health as a result of the DE. Additionally, the DE can improve residents' health through the promotion of regional green development. The study's findings add to our knowledge of how the DE impacts residents' health while also offering recommendations for achieving universal health.


Subject(s)
Economic Development , Public Policy , China
2.
Cell Death Dis ; 14(1): 53, 2023 01 21.
Article in English | MEDLINE | ID: mdl-36681663

ABSTRACT

Obesity is a risk factor in various types of cancer, including breast cancer. The disturbance of adipose tissue in obesity highly correlates with cancer progression and resistance to standard treatments such as chemo- and radio-therapies. In this study, in a syngeneic mouse model of triple-negative breast cancer (TNBC), diet-induced obesity (DIO) not only promoted tumor growth, but also reduced tumor response to radiotherapy. Serpine1 (Pai-1) was elevated in the circulation of obese mice and was enriched within tumor microenvironment. In vitro co-culture of human white adipocytes-conditioned medium (hAd-CM) with TNBC cells potentiated the aggressive phenotypes and radioresistance of TNBC cells. Moreover, inhibition of both cancer cell autonomous and non-autonomous SERPINE1 by either genetic or pharmacological strategy markedly dampened the aggressive phenotypes and radioresistance of TNBC cells. Mechanistically, we uncovered a previously unrecognized role of SERPINE1 in DNA damage response. Ionizing radiation-induced DNA double-strand breaks (DSBs) increased the expression of SERPINE1 in cancer cells in an ATM/ATR-dependent manner, and promoted nuclear localization of SERPINE1 to facilitate DSB repair. By analyzing public clinical datasets, higher SERPINE1 expression in TNBC correlated with patients' BMI as well as poor outcomes. Elevated SERPINE1 expression and nuclear localization were also observed in radioresistant breast cancer cells. Collectively, we reveal a link between obesity and radioresistance in TNBC and identify SERPINE1 to be a crucial factor mediating obesity-associated tumor radioresistance.


Subject(s)
Triple Negative Breast Neoplasms , Animals , Mice , Humans , Triple Negative Breast Neoplasms/genetics , Triple Negative Breast Neoplasms/radiotherapy , Triple Negative Breast Neoplasms/drug therapy , Cell Line, Tumor , DNA Repair , Obesity/genetics , Obesity/complications , DNA Breaks, Double-Stranded , Tumor Microenvironment , Plasminogen Activator Inhibitor 1/genetics
3.
Biomedicines ; 10(5)2022 May 23.
Article in English | MEDLINE | ID: mdl-35625948

ABSTRACT

Cellular stress response is an important adaptive mechanism for regulating cell fate decision when cells confront with stress. During tumorigenesis, tumor progression and the course of treatment, cellular stress signaling can activate subsequent response to deal with stress. Therefore, cellular stress response has impacts on the fate of tumor cells and tumor responsiveness relative to therapeutic agents. In recent years, attention has been drawn to long non-coding RNAs (lncRNAs), a novel class of RNA molecules with more than 200 nucleotides in length, which has little protein-coding potential and possesses various functions in multiple biological processes. Accumulating evidence has shown that lncRNAs are also engaged in the regulation of cellular stress response, particularly in cancers. Here, we summarize lncRNAs that have been reported in the adaptive response to major types of cellular stress including genotoxic, hypoxic, oxidative, metabolic and endoplasmic reticulum stress, all of which are often encountered by cancer cells. Specifically, the molecular mechanisms of how lncRNAs regulate cellular stress response during tumor progression or the development of therapy resistance are emphasized. The potential clinical applications of stress-responsive lncRNAs as biomarkers will also be discussed.

4.
FASEB J ; 36(3): e22201, 2022 03.
Article in English | MEDLINE | ID: mdl-35137449

ABSTRACT

Oncogene activation, massive proliferation, and increased nutrient demands often result in nutrient and oxygen deprivation in solid tumors including breast cancer (BC), leading to the induction of oxidative stress and endoplasmic reticulum (ER) stress, and subsequently triggering integrated stress response (ISR). To elucidate the role of long non-coding RNAs (lncRNAs) in the ISR of BC, we performed transcriptome analyses and identified a lncRNA, UBA6-AS1, which was upregulated upon amino acid deprivation and ER stress. UBA6-AS1 was preferentially induced in triple-negative BC (TNBC) cells deprived of arginine or glutamine, two critical amino acids required for cancer cell growth, or treated with ER stress inducers. Mechanistically, UBA6-AS1 was regulated through the GCN2/eIF2α/ATF4 pathway, one of the major routes mediating ISR in amino acid sensing. In addition, both in vitro and in vivo assays indicated that UBA6-AS1 promoted TNBC cell survival when cells encountered metabolic stress, implicating a regulatory role of UBA6-AS1 in response to intratumoral metabolic stress during tumor progression. Moreover, PARP1 expression and activity were positively regulated by the GCN2/UBA6-AS1 axis upon amino acid deprivation. In conclusion, our data suggest that UBA6-AS1 is a novel lncRNA regulating ISR upon metabolic stress induction to promote TNBC cell survival. Furthermore, the GCN2-ATF4 axis is important for UBA6-AS1 induction to enhance PARP1 activity and could serve as a marker for the susceptibility of PARP inhibitors in TNBC.


Subject(s)
Amino Acids/deficiency , Endoplasmic Reticulum Stress , Protein Serine-Threonine Kinases/metabolism , Triple Negative Breast Neoplasms/metabolism , Activating Transcription Factor 4/genetics , Activating Transcription Factor 4/metabolism , Amino Acids/metabolism , Animals , Female , HEK293 Cells , Humans , MCF-7 Cells , Mice , Mice, Inbred NOD , Mice, SCID , Protein Serine-Threonine Kinases/genetics , RNA, Antisense , Triple Negative Breast Neoplasms/genetics
5.
Sci Rep ; 10(1): 13582, 2020 08 12.
Article in English | MEDLINE | ID: mdl-32788720

ABSTRACT

In many human cancers, including hepatocellular carcinoma (HCC), high density of infiltrating tumor-associated macrophages (TAM) is associated with poor prognosis. Most TAMs express a M2 phenotype subsequently supporting tumor growth. How tumor cells polarize these TAMs to a pro-tumor M2 phenotype is still poorly understood. Our previous studies have revealed that a Toll-like receptor 2 (TLR2)-dependent autophagy triggered by hepatoma-derived factors down-regulates NF-κB p65 and drives M2 macrophage differentiation. However, the underlying mechanisms and potential hepatoma-derived TLR2 ligands are not clear. Here, we provide evidence to reveal that NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS) generation is crucial for HCC-induced autophagy, NF-κB p65 down-regulation and M2 phenotype polarization in primary macrophages. This NOX2-generated ROS production in abolished in TLR2-deficient macrophages. HCC-derived or recombinant high-mobility group box 1 (HMGB1) is able to trigger this TLR2-mediated M2 macrophage polarization. Blockage of HMGB1 and ROS by inhibitors, ethyl pyruvate and N-acetylcysteine amide, respectively, significantly reduces both M2 macrophage accumulation and liver nodule formation in HCC-bearing mice. Our findings uncover a HMGB1/TLR2/NOX2/autophagy axis to trigger M2 macrophage polarization in HCC that can be considered as a novel therapeutic target for treating HCC.


Subject(s)
Autophagy , Carcinoma, Hepatocellular/metabolism , HMGB1 Protein/metabolism , Liver Neoplasms/metabolism , Macrophages/metabolism , NADPH Oxidase 2/metabolism , Toll-Like Receptor 2/metabolism , Animals , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , Cells, Cultured , HEK293 Cells , Humans , Liver Neoplasms/pathology , Macrophage Activation , Macrophages/classification , Mice, Inbred BALB C , Mice, Inbred C57BL , Mice, Knockout , Signal Transduction , Toll-Like Receptor 2/genetics
6.
Plant J ; 94(4): 612-625, 2018 05.
Article in English | MEDLINE | ID: mdl-29495079

ABSTRACT

Rice (Oryza sativa L.) has two ecotypes, upland and lowland rice, that have been observed to show different tolerance levels under flooding stress. In this study, two rice cultivars, upland (Up221, flooding-intolerant) and lowland (Low88, flooding-tolerant), were initially used to study their molecular mechanisms in response to flooding germination. We observed that variations in the OsCBL10 promoter sequences in these two cultivars might contribute to this divergence in flooding tolerance. Further analysis using another eight rice cultivars revealed that the OsCBL10 promoter could be classified as either a flooding-tolerant type (T-type) or a flooding-intolerant type (I-type). The OsCBL10 T-type promoter only existed in japonica lowland cultivars, whereas the OsCBL10 I-type promoter existed in japonica upland, indica upland and indica lowland cultivars. Flooding-tolerant rice cultivars containing the OsCBL10 T-type promoter have shown lower Ca2+ flow and higher α-amylase activities in comparison to those in flooding-intolerant cultivars. Furthermore, the OsCBL10 overexpression lines were sensitive to both flooding and hypoxic treatments during rice germination with enhanced Ca2+ flow in comparison to wild-type. Subsequent findings also indicate that OsCBL10 may affect OsCIPK15 protein abundance and its downstream pathways. In summary, our results suggest that the adaptation to flooding stress during rice germination is associated with two different OsCBL10 promoters, which in turn affect OsCBL10 expression in different cultivars and negatively affect OsCIPK15 protein accumulation and its downstream cascade.


Subject(s)
Adaptation, Physiological , Calcineurin/metabolism , Calcium/metabolism , Oryza/genetics , Promoter Regions, Genetic/genetics , Calcineurin/genetics , Ecotype , Floods , Genetic Variation , Germination , Oryza/physiology , Plant Proteins/genetics , Plant Proteins/metabolism , Protein Kinases/genetics , Protein Kinases/metabolism , Seeds/genetics , Seeds/physiology , Species Specificity , Stress, Physiological
7.
Compr Psychiatry ; 55(3): 688-92, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24355706

ABSTRACT

OBJECTIVE: The present study examined the relation between déjà vu experiences and paranormal beliefs in schizophrenic patients. METHODS: A total of 522 participants (54.5% female; mean age=33.3, SD=16.02) were recruited, including 422 healthy adults (60.9% female; mean age=29.48, SD=15.07) and 100 medicated adult schizophrenic patients (27.3% female; mean age=48.98, SD=8.57). The Chinese version of the Inventory of Déjà-vu Experiences Assessment was created via back translation. Chinese versions of the Revised Paranormal Belief Scale (CRPB), Beck Anxiety Inventory (CBAI), and Perceived Stress Scale (CPSS) were also used. RESULTS AND CONCLUSION: After controlling for age, gender, education, and anxiety, the results supported the following three hypotheses. Schizophrenic persons have fewer déjà vu experiences than normal persons. These experiences are positively related to paranormal beliefs in healthy adults but not in schizophrenic patients. Schizophrenic patients have higher scores than healthy adults on the psi and superstitious subscales of the CRPB.


Subject(s)
Antipsychotic Agents/therapeutic use , Culture , Deja Vu , Schizophrenia/drug therapy , Schizophrenic Psychology , Superstitions , Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult
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