A Review of Research Progress on the Mechanisms of Programmed Nerve Cell Death.

Objective: This study aimed to review recent advancements in understanding neural programmed cell death (PCD) mechanisms, providing valuable insights for clinical research. Methods: The review involves an in-depth analysis of the literature on neural PCD, encompassing studies conducted in recent years. The methodology includes an extensive examination of research findings and their implications. Results: The review suggested that PCD is a process characterized by the early degradation of cellular deoxyribonucleic acid (DNA) triggered by specific factors or signals. It plays a significant role during organism development. PCD comprises two primary forms: programmed necrosis and apoptosis. Apoptosis is caspase-dependent and well-defined in terms of signaling pathways, whereas programmed necrosis is caspase-independent, and its signaling pathways remain unclear. Maintaining intracellular equilibrium is vital, and PCD follows a comprehensive process involving activation, transference, and apoptosis stages. Specific genes regulate this process, leading to the production of lethal proteins. However, the precise mechanisms remain incompletely understood, warranting further exploration. Conclusions: This review sheds light on the intricate mechanisms of neural PCD. While substantial progress has been made, many aspects still require in-depth investigation. The findings offer a valuable foundation for future clinical research in this field.

Genome-Wide Identification of NAC Gene Family and Expression Analysis under Abiotic Stresses in Avena sativa.

In this study, a total of 177 NAC members were identified in Avena sativa, located on 21 chromosomes. Phylogenetic analysis showed that AsNAC proteins could be divided into seven subfamilies (I-VII), and that proteins in the same subfamily have similar protein motifs. Gene structure analysis found that NAC introns ranged from 1 to 17. Cis-element analysis of the promoter indicated that the gene family may have stress-related elements and growth regulation elements. Through qRT-PCR experiments, we speculated that AsNACs genes can respond to abiotic stresses such as cold, freezing, salt, and saline alkali. This study provides a theoretical basis for further exploring the function of the NAC gene family in A. sativa.

Genome-Wide Analysis and Expression of the GRAS Transcription Factor Family in Avena sativa.

The GRAS transcription factor is an important transcription factor in plants. In recent years, more GRAS genes have been identified in many plant species. However, the GRAS gene family has not yet been studied in Avena sativa. We identified 100 members of the GRAS gene family in A. sativa (Avena sativa), named them AsGRAS1~AsGRAS100 according to the positions of 21 chromosomes, and classified them into 9 subfamilies. In this study, the motif and gene structures were also relatively conserved in the same subfamilies. At the same time, we found a great deal related to the stress of cis-acting promoter regulatory elements (MBS, ABRE, and TC-rich repeat elements). qRT-PCR suggested that the AsGRAS gene family (GRAS gene family in A. sativa) can regulate the response to salt, saline-alkali, and cold and freezing abiotic stresses. The current study provides original and detailed information about the AsGRAS gene family, which contributes to the functional characterization of GRAS proteins in other plants.

Compositions and Co-occurrence Patterns of Bacterial Communities Associated With Polymer- and ASP-Flooded Petroleum Reservoir Blocks.

Polymer flooding technology and alkaline-surfactant-polymer (ASP) flooding technology have been widely used in some oil reservoirs. About 50% of remaining oil is trapped, however, in polymer-flooded and ASP-flooded reservoirs. How to further improve oil recovery of these reservoirs after chemical flooding is technically challenging. Microbial enhanced oil recovery (MEOR) technology is a promising alternative technology. However, the bacterial communities in the polymer-flooded and ASP-flooded reservoirs have rarely been investigated. We investigated the distribution and co-occurrence patterns of bacterial communities in ASP-flooded and polymer-flooded oil production wells. We found that Arcobacter and Pseudomonas were dominant both in the polymer-flooded and ASP-flooded production wells. Halomonas accounted for a large amount of the bacterial communities inhabiting in the ASP-flooded blocks, whereas they were hardly detected in the polymer-flooded blocks, and the trends for Acetomicrobium were the opposite. RDA analysis indicated that bacterial communities in ASP-flooded and polymer-flooded oil production wells are closely related to the physical and chemical properties, such as high salinity and strong alkaline, which together accounted for 56.91% of total variance. Co-occurrence network analysis revealed non-random combination patterns of bacterial composition from production wells of ASP-flooded and polymer-flooded blocks, and the ASP-flooded treatment decreased bacterial network complexity, suggesting that the application of ASP flooding technology reduced the tightness of bacterial interactions.

Geodermatophilus daqingensis sp. nov., isolated from petroleum-contaminated soil.

A novel Gram-positive actinobacterium, designated WT-2-1T, was isolated from a sample of petroleum-contaminated soil collected in Daqing, Heilongjiang province, China and characterised using a polyphasic taxonomic approach. The optimal growth for strain WT-2-1T was found to be at 25-35 °C and at pH 6.0-9.0 and with 0-4% (w/v) NaCl, forming blackish green-coloured colonies. Chemotaxonomic and molecular characteristics of the isolate match those described for members of the genus Geodermatophilus. The peptidoglycan was found to contain meso-diaminopimelic acid; galactose, glucose and xylose were detected as diagnostic sugars. The main phospholipids were identified as diphosphatidylglycerol, phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine and phosphatidylglycerol; MK-9(H4) was the dominant menaquinone present. The major cellular fatty acids were identified as iso-C16:0 and iso-C15:0. 16S rRNA gene sequence analysis showed that strain WT-2-1T is a member of the genus Geodermatophilus, with high sequence similarities to Geodermatophilus aquaeductus BMG801T (98.4%), Geodermatophilus saharensis CF5/5T (98.4%), Geodermatophilus bullaregiensis BMG841T (98.3%) and Geodermatophilus normandii CF5/3T (98.3%). Based on the phenotypic characteristics, phylogenetic data and DNA-DNA hybridization results, the isolate is concluded to represent a novel species of the genus Geodermatophilus, for which the name Geodermatophilus daqingensis sp. nov. is proposed. The type strain is WT-2-1T (=CGMCC 4.7381T = DSM 104001T).

ATRA inhibits the proliferation of DU145 prostate cancer cells through reducing the methylation level of HOXB13 gene.

All-trans retinoic acid (ATRA) has been widely investigated for treatments of many cancers including prostate cancer. HOXB13, silenced in androgen receptor-negative (AR(-)) prostate cancer cells, plays a role in AR(-) prostate cancer cell growth arrest. In this study we intended to elucidate the mechanisms that are involved in the proliferation inhibition of AR(-) prostate cancer cells triggered by ATRA. We discovered that ATRA was able to induce the growth arrest and to increase HOXB13 expression in AR(-) prostate cancer cells. Both EZH2 and DNMT3b participated in the repression of HOXB13 expression through an epigenetic mechanism involving DNA and histone methylation modifications. Specifically, EZH2 recruited DNMT3b to HOXB13 promoter to form a repression complex. Moreover, ATRA could upregulate HOXB13 through decreasing EZH2 and DNMT3b expressions and reducing their interactions with the HOXB13 promoter. Concurrently, the methylation level of the HOXB13 promoter was reduced upon the treatment of ATRA. Results from this study implicated a novel effect of ATRA in inhibition of the growth of AR(-) resistant human prostate cancer cells through alteration of HOXB13 expression as a result of epigenetic modifications.

BMP4-Smad signaling pathway mediates adriamycin-induced premature senescence in lung cancer cells.

Cell senescence, an irreversible cell cycle arrest, reflects a safeguard program that limits the capacity of uncontrolled cell proliferation. Treatment of tumor cells with certain chemotherapeutic agents activates premature senescence to decrease the tumorigenecity. Here we show that sublethal concentrations of adriamycin could induce premature senescence in lung cancer cells. Adriamycin treatment resulted in the up-regulation of BMP4, which is underexpressed in NSCLC (non-small cell lung cancers). Moreover, the BMP4-Smad pathway played a key role in mediating adriamycin-induced senescence. Overexpression of BMP4 was able to induce premature senescence in lung cancer cells and this process required the participation of cyclin/cyclin-dependent kinase (cdk) inhibitors p16(INK4a) and p21(WAF1/cip1). We also show that increases of p16(INK4a) and p21(WAF1/cip1) expression in response to BMP4 were mediated by the Smad signaling pathway. Furthermore, our data revealed that p300 was recruited to P16(INK4a) and P21(WAF1/cip1) promoters by Smad1/5/8 to induce the hyperacetylation of histones H3 and H4 at the promoters. The present study provides useful clues to the evaluation of the potentiality of BMP4 as a responsive molecular target for cancer chemotherapy.

SOX7, down-regulated in colorectal cancer, induces apoptosis and inhibits proliferation of colorectal cancer cells.

The sex-determining region Y-box 7 (Sox7) is a member of high mobility group (HMG) transcription factor family, essential for embryonic development and endoderm differentiation. Deregulation of Wnt signaling pathway is a hallmark of colorectal cancer. Our results showed that the expression level of SOX7 was frequently down-regulated in human colorectal cancer cell lines and in primary colorectal tumor tissues, and the SOX7 silencing was partially due to the aberrant DNA methylation of the gene. Restoration of SOX7 induced colorectal cancer cell apoptosis, inhibited cell proliferation and colony formation. In addition, SOX7 efficiently suppressed beta-catenin-mediated transcriptional activity.

Recruitment of HDAC4 by transcription factor YY1 represses HOXB13 to affect cell growth in AR-negative prostate cancers.

HOXB13 is a homeodomain protein implicated to play a role in growth arrest in AR (androgen receptor)-negative prostate cancer cells. Expression of HOXB13 is restricted to the AR-expressing prostate cells. In this report, we demonstrate that the HDAC inhibitor NaB (sodium butyrate) was able to induce cell growth arrest and to increase HOXB13 expression in AR-negative prostate cancer cells. We also show that both HDAC4 and YY1 participated in the repression of HOXB13 expression through an epigenetic mechanism involving histone acetylation modification. Specifically, co-immunoprecipitation assays revealed that HDAC4 and YY1 formed a complex. The chromatin immunoprecipitation (ChIP) assays verified that HDAC4 was recruited to HOXB13 promoter by YY1. Moreover, promoter truncation and point mutation studies determined that the two proximal YY1 binding sites on the HOXB13 promoter were essential for the recruitments of YY1 and HDAC4. Data presented in this report suggest that YY1 and HDAC4 affected cell growth by repressing transcriptional regulation of HOXB13 through an epigenetic modification of histones.

YY1 restrained cell senescence through repressing the transcription of p16.

The transcription factor YY1 has been implicated to play a role in cell growth control. In this report, we demonstrate that YY1 was able to suppress NCI-H460 cell senescence through regulating the expression of p16(INK4a), a cyclin-dependent kinase inhibitor. We also show that YY1 participated in the repression of p16(INK4a) expression in 293T cells through an epigenetic mechanism involving histone acetylation modification. Specifically, HDAC3 and HDAC4 inhibited the p16(INK4a) promoter activity. The chromatin immunoprecipitation (ChIP) assays verified that HDAC3 and HDAC4 were recruited to p16(INK4a) promoter by YY1. Moreover, co-immunoprecipitation assays revealed that these three protein factors formed a complex. Furthermore, knockdown of these factors induced cell enlargement and flattened morphology and significantly increased the SA-beta-gal activity, a biochemical marker of cell senescence. Overall, data from this study suggest that YY1, HDAC3 and HDAC4 restrained cell senescence by repressing p16(INK4a) expression through an epigenetic modification of histones.