Search

Tangeretin (Tan), a citrus flavonoid, possesses a strong anti-tumor efficacy in various human cancers. However, the precise role of Tan in the development of esophageal squamous cell carcinoma (ESCC) remains unclear. RNA sequencing (RNA-seq) analysis was performed to observe the Tan-related genes in Tan-treated TE-1 cells. The direct relationship between GLI family zinc finger 2 (GLI2) and the promoter of glycoprotein non-metastatic melanoma protein B (GPNMB) was predicted by bioinformatics analysis and validated by luciferase reporter and chromatin immunoprecipitation (ChIP) assays. Cell survival after Tan treatment was assessed by CCK8 assay. Gene expression levels were evaluated by a qRT-PCR, western blot, or immunofluorescence method. Cell migration and invasion were detected by wound-healing and transwell assays. The function of Tan in vivo was examined using xenograft studies. Our data indicated anti-migration and anti-invasion functions of Tan in ESCC cells in vitro. Tan also diminished tumor growth in vivo. Mechanistically, Tan diminished the expression and transcriptional activity of GLI2 in ESCC cells. Silencing of GLI2 resulted in decreased expression of GPNMB by inhibiting GPNMB transcription via the binding site at the GPNMB promoter at position +(1539–1550). Moreover, Tan down-regulated GPNMB expression in ESCC cells, and re-expression of GPNMB reversed anti-migration and anti-invasion functions of Tan in ESCC cells. Our findings uncover anti-migration and anti-invasion effects of Tan in ESCC cells by down-regulating GPNMB by suppressing GLI2-mediated GPNMB transcription, providing new evidence that Tan can function as a therapeutic agent against ESCC. [ABSTRACT FROM AUTHOR]

Background: In the ICU ward, septic cirrhotic patients are susceptible to suffering from sepsis-associated encephalopathy and/or hepatic encephalopathy, which are two common neurological complications in such patients. However, the mutual pathogenesis between sepsis-associated and hepatic encephalopathies remains unclear. We aimed to identify the mutual hub genes, explore effective diagnostic biomarkers and therapeutic targets for the two common encephalopathies and provide novel, promising insights into the clinical management of such septic cirrhotic patients. Methods: The precious human post-mortem cerebral tissues were deprived of the GSE135838, GSE57193, and GSE41919 datasets, downloaded from the Gene Expression Omnibus database. Furthermore, we identified differentially expressed genes and screened hub genes with weighted gene co-expression network analysis. The hub genes were then subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway functional enrichment analyses, and protein-protein interaction networks were constructed. Receiver operating characteristic curves and correlation analyses were set up for the hub genes. Finally, we explored principal and common signaling pathways by using Gene Set Enrichment Analysis and the association between the hub genes and immune cell subtype distribution by using CIBERSORT algorithm. Results: We identified seven hub genes—GPR4, SOCS3, BAG3, ZFP36, CDKN1A, ADAMTS9, and GADD45B—by using differentially expressed gene analysis and weighted gene co-expression network analysis method. The AUCs of these genes were all greater than 0.7 in the receiver operating characteristic curves analysis. The Gene Set Enrichment Analysis results demonstrated that mutual signaling pathways were mainly enriched in hypoxia and inflammatory response. CIBERSORT indicated that these seven hub genes were closely related to innate and adaptive immune cells. Conclusions: We identified seven hub genes with promising diagnostic value and therapeutic targets in septic cirrhotic patients with sepsis-associated encephalopathy and/or hepatic encephalopathy. Hypoxia, inflammatory, and immunoreaction responses may share the common downstream pathways of the two common encephalopathies, for which earlier recognition and timely intervention are crucial for management of such septic cirrhotic patients in ICU. [ABSTRACT FROM AUTHOR]

Postmenopausal women experience several symptoms, including inflammation and a sharp rise in oxidative stress caused by estrogen deprivation. Although estrogen replacement therapy (ERT) is generally regarded as an effective treatment for menopause, it has been used less frequently due to some adverse effects and high costs. Therefore, there is an immediate need to develop an effective herbal-based treatment that is affordable for low-income populations. Acordingly, this study explored the estrogen-like properties of methanol extracts from Cynanchum wilfordii (CW) and Poligonum multiflorum (PM), two important medicinal plants in Republic of Korea, Japan, and China. Due to the similar names and morphologies of these two radixes, they are frequently confused in the marketplace. Our previous colleagues discriminated between these two plants. In this study, we investigated the estrogenic activity of PM and CW using several in vitro assays with their possible mechanism of action. First, their phytochemical contents, such as gallic acid, 2,3,5,4′-tetrahydroxystilbene-2-O-glucoside (TSG) and emodin, were quantified using high-performance liquid chromatography (HPLC). Secondly, estrogen-like activity was assessed utilizing the well-known E-screen test and gene expression analysis in estrogen receptor (ER)-positive MCF7 cells. ROS inhibition and anti-inflammatory effects were analyzed using HaCaT and Raw 264.7 cells, respectively. Our findings demonstrate that PM extracts significantly increased the expression of the estrogen-dependent genes (ERα, ERβ, pS2) and boosted MCF7 cell proliferation in comparison to CW extracts. Additionally, PM extract demonstrated a significant reduction in reactive oxygen species (ROS) production as well as an enhanced antioxidant profile compared to the CW extract. Further, the PM extract treatment significantly reduced the generation of nitric oxide (NO) in RAW 264.7 cells, a murine macrophage cell line, demonstrating the anti-inflammatory properties of the extract. Finally, this research offers an experimental foundation for the use of PM as a phytoestrogen to minimize menopausal symptoms. [ABSTRACT FROM AUTHOR]

[Display omitted] Neuropathic pain is chronic pain caused by a lesion or disease of the somatosensory nervous system. Neuropathic pain, with a high incidence and complex pathogenesis, is one of the most significant areas of clinical medicine and basic research. Currently, prescribed treatments are still unsatisfactory or have limited effectiveness. A medicinal preparation is required that relieves the neuropathic pain and prolongs action time, which has not yet been discovered. In this study, MIL-101 (Fe) was employed as a drug carrier to regulate the release of diclofenac sodium, thereby achieving the effect of analgesia and sustained release. The release curves demonstrated that diclofenac sodium could be continuously released from MIL-101 (Fe) for more than 48 h. There was no toxicity in vitro and in vivo, and the safety of MIL-101 (Fe) was confirmed by hematoxylin and eosin as well as ELISA tests in vivo. The results of behavioral testing, pharmacokinetics, and RNA sequencing analysis showed that MIL-101 (Fe) loaded with diclofenac sodium could enhance the mechanical withdrawal threshold and alleviate cold allodynia induced by Spared Nerve Injury, prolonging the work time by three days. The results indicated that MIL-101 (Fe) exhibited excellent biocompatibility, while the MIL-101 (Fe)-DS demonstrated analgesic and controlled-release properties. These findings provide a scientific foundation for the clinical management of neuropathic pain and the development of a novel formulation. [ABSTRACT FROM AUTHOR]

Objective. Endothelial cell-specific molecule 1 (ESM1) has been implicated as an oncogene in several types of cancer. However, the potential role of ESM1 in esophageal carcinogenesis (ESCA)/esophageal squamous cell carcinoma (ESCC) is still unclear. Methods. The expression, function, and survival data of ESM1 were observed using a bioinformatics approach. Subsequently, the expression level of ESM1 in surgical esophageal tumors and adjacent normal tissues was detected by qRT–PCR and immunofluorescence. We further revealed protein expression by immunohistochemistry (IHC), which is related to the prognosis of patients with ESCC using survival analysis. In vitro, knockdown of ESM1 in KYSE150 and KYSE510 cell lines, colony formation assays, wound healing assays, and Transwell assays were performed. Results. ESM1 is significantly elevated in 12 of 20 types of human cancer. ESM1 is highly expressed in tumor tissue compared with adjacent normal tissue and was identified as a hub gene in ESCA. Clinical outcome endpoints of overall survival (OS), progression-free interval (PFI), and disease-specific survival (DSS) curves showed that patients whose ESM1 expression was high had a lower clinical survival rate. The ESM1 high-expression group has a certain correlation with clinical stage and grade. The IHC of ESM1 further demonstrated that the higher the expression was, the worse the N classification and pTNM stage in patients with ESCC, which had a distinctly poorer overall 5-year survival rate. Univariate analysis showed that age, N classification, pTNM stage, and ESM1 expression were all prognostic factors, although multivariate Cox regression analysis showed that only pTNM stage was an independent prognostic factor. In vitro, silencing ESM1 suppressed the proliferation, migration, and invasion of KYSE150 and KYSE510 cells. Conclusions. ESM1 is a hub gene in the initiation and progression of ESCA/ESCC that promotes the proliferation, migration, and invasion of esophageal cancer cells and may be a promising therapeutic target and prognostic indicator. [ABSTRACT FROM AUTHOR]

Two new unsymmetrical ligands, namely, 2-(pyridin-3-yl)-5-(quinolin-2-yl)-1,3,4-oxadiazole (L1) and 2-(pyridin-4-yl)-5-(quinolin-2-yl)-1,3,4-oxadiazole (L2), have been synthesized and their self-assembly reactions with Co(NO3)2 and Co(ClO4)2 have been investigated for the rational construction of coordination polymers (CPs). It was found that the counter-anion plays an important role in the structural assemblies. Their anti-ovarian cancer activity was evaluated and the related mechanism was explored at the same time. Firstly, the proliferation of the ovarian cancer cells was measured with CCK-8 detection kit. Then, the real time RT-PCR was used to evaluate the relative expression levels of the ROS related genes in the ovarian cancer cells after compounds treatment. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is a debilitating psychiatric disorder which is common and endangers human physical and mental health. Studies have shown that hesperidin could improve the symptoms of depression with unclear mechanisms. In this study, hesperidin was administered to chronic unpredictable mild stress (CUMS) depressed mice before behavioral test, network pharmacology analysis, RNA expression microarray analysis, pathway validation and molecular docking experiments. we found that hesperidin intervention could significantly improve the depressive symptoms and downregulate the expression level of pyroptosis pathway including caspase 1 (Casp1), interleukin 18 (IL18), interleukin-1β (IL-1β) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3). In addition, we found that hesperidin could possibly bind to NLRP3. Our study demonstrated that hesperidin had huge potential as anti-depressive neuroprotectant, and may play a role in treating MDD by regulating NLRP3-mediated pyroptosis. [ABSTRACT FROM AUTHOR]

Catalytically inactive CRISPR‐Cas13 (dCas13)‐based base editors can achieve the conversion of adenine‐to‐inosine (A‐to‐I) or cytidine‐to‐uridine (C‐to‐U) at the RNA level, however, the large size of dCas13 protein limits its in vivo applications. Here, a compact and efficient RNA base editor (ceRBE) is reported with high in vivo editing efficiency. The larger dCas13 protein is replaced with a 199‐amino acid EcCas6e protein, derived from the Class 1 CRISPR family involved in pre‐crRNA processing, and conducted optimization for toxicity and editing efficiency. The ceRBE efficiently achieves both A‐to‐I and C‐to‐U base editing with low transcriptome off‐target in HEK293T cells. The efficient repair of the DMD Q1392X mutation (68.3±10.1%) is also demonstrated in a humanized mouse model of Duchenne muscular dystrophy (DMD) after AAV delivery, achieving restoration of expression for gene products. The study supports that the compact and efficient ceRBE has great potential for treating genetic diseases. [ABSTRACT FROM AUTHOR]

SUMMARY: As a plant‐specific transcription factor, lateral organ boundaries domain (LBD) protein was reported to regulate plant growth and stress response, but the functional research of subfamily II genes is limited. SlMYC2, a master regulator of Jasmonic acid response, has been found to exhibit high expression levels in fruit and has been implicated in the regulation of fruit ripening and resistance to Botrytis. However, its role in fruit expansion remains unknown. In this study, we present evidence that a subfamily II member of LBD, namely SlLBD40, collaborates with SlMYC2 in the regulation of fruit expansion. Overexpression of SlLBD40 significantly promoted fruit growth by promoting mesocarp cell expansion, while knockout of SlLBD40 showed the opposite result. Similarly, SlMYC2 knockout resulted in a significant decrease in cell expansion within the fruit. Genetic analysis indicated that SlLBD40‐mediated cell expansion depends on the expression of SlMYC2. SlLBD40 bound to the promoter of SlEXPA5, an expansin gene, but did not activate its expression directly. While, the co‐expression of SlMYC2 and SlLBD40 significantly stimulated the activation of SlEXPA5, leading to an increase in fruit size. SlLBD40 interacted with SlMYC2 and enhanced the stability and abundance of SlMYC2. Furthermore, SlMYC2 directly targeted and activated the expression of SlLBD40, which is essential for SlLBD40‐mediated fruit expansion. In summary, our research elucidates the role of the interaction between SlLBD40 and SlMYC2 in promoting cell expansion in tomato fruits, thus providing novel insights into the molecular genetics underlying fruit growth. [ABSTRACT FROM AUTHOR]

Tardigrades, commonly known as water bears, are enigmatic organisms characterized by their remarkable resilience to extreme environments despite their simple and compact body structure. To date, there is still much to understand about their evolutionary and developmental features contributing to their special body plan and abilities. This research provides preliminary insights on the conserved and specific gene expression patterns during embryonic development of water bears, focusing on the species Hypsibius exemplaris. The developmental dynamic expression analysis of the genes with various evolutionary age grades indicated that the mid‐conserved stage of H. exemplaris corresponds to the period of ganglia and midgut development, with the late embryonic stage showing a transition from non‐conserved to conserved state. Additionally, a comparison with Drosophila melanogaster highlighted the absence of certain pathway nodes in development‐related pathways, such as Maml and Hairless, which are respectively the transcriptional co‐activator and co‐repressor of NOTCH regulated genes. We also employed Weighted Gene Co‐expression Network Analysis (WGCNA) to investigate the expression patterns of tardigrade‐specific genes during embryo development. Our findings indicated that the module containing the highest proportion of tardigrade‐specific genes (TSGs) exhibits high expression levels before the mid‐conserved stage, potentially playing a role in glutathione and lipid metabolism. These functions may be associated to the ecdysone synthesis and storage cell formation, which is unique to tardigrades. [ABSTRACT FROM AUTHOR]

Human adipose-derived stem cells (ADSCs) have become a promising therapeutic approach against skin aging. Recent studies confirm that exosomes partially mediate the therapeutic effect of stem cells. This study successfully isolated exosomes from the ADSC culture medium and discovered that ADSC-derived exosomes (ADSC-Exos) could alleviate human dermal fibroblast (HDF) senescence and stimulate HDF migration. Moreover, ADSC-Exos increased the type I collagen expression level and reduced the reactive oxygen species (ROS) and senescence-associated β-galactosidase (SA-β-Gal) activity in HDFs. In addition, we demonstrated that ADSC-Exos significantly inhibited senescence-related protein expression levels of p53, p21, and p16. In conclusion, our results have revealed the antisenescence effects of ADSC-Exos on HDFs and ADSC-Exos may be a novel cell-free therapeutic tool for antiaging. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction is considered to be an important mediator of the pro‐aging process in chronic kidney disease, which is continuously increasing worldwide. Although PTEN‐induced kinase 1 (PINK1) regulates mitochondrial function, its role in renal aging remains unclear. We investigated the association between PINK1 and renal aging, especially through the cGAS‐STING pathway, which is known to result in an inflammatory phenotype. Pink1 knockout (Pink1−/−) C57BL/6 mice and senescence‐induced renal tubular epithelial cells (HKC‐8) treated with H2O2 were used as the renal aging models. Extensive analyses at transcriptomic‐metabolic levels have explored changes in mitochondrial function in PINK1 deficiency. To investigate whether PINK1 deficiency affects renal aging through the cGAS‐STING pathway, we explored their expression levels in PINK1 knockout mice and senescence‐induced HKC‐8 cells. PINK1 deficiency enhances kidney fibrosis and tubular injury, and increases senescence and the senescence‐associated secretory phenotype (SASP). These phenomena were most apparent in the 24‐month‐old Pink1−/− mice and HKC‐8 cells treated with PINK1 siRNA and H2O2. Gene expression analysis using RNA sequencing showed that PINK1 deficiency is associated with increased inflammatory responses, and transcriptomic and metabolomic analyses suggested that PINK1 deficiency is related to mitochondrial metabolic dysregulation. Activation of cGAS‐STING was prominent in the 24‐month‐old Pink1−/− mice. The expression of SASPs was most noticeable in senescence‐induced HKC‐8 cells and was attenuated by the STING inhibitor, H151. PINK1 is associated with renal aging, and mitochondrial dysregulation by PINK1 deficiency might stimulate the cGAS‐STING pathway, eventually leading to senescence‐related inflammatory responses. [ABSTRACT FROM AUTHOR]

GINS2 is overexpressed in several cancers, but little is known about its role in osteosarcoma (OS). A series of in vivo and in vitro experiments were conducted to explore the role of GINS2 in OS. In this study, we demonstrated that GINS2 was found to be highly expressed in OS tissues and cell lines, which was associated with poor outcomes in OS patients. GINS2 knockdown hindered the growth and induced apoptosis in OS cell lines in vitro. Furthermore, GINS2 knockdown effectively inhibited the growth of a xenograft tumor in vivo. By using an Affymetrix gene chip and intelligent pathway analysis, it was demonstrated that the GINS2 knockdown could reduce the expression of several targeted genes and reduce the activity of the MYC signaling pathway. Mechanically, LC-MS, CoIP, and rescue experiments revealed that GINS2 promoted tumor progression through the STAT3/MYC axis in the OS. Moreover, GINS2 was associated with tumor immunity and may be a potential immunotherapeutic target for OS. [ABSTRACT FROM AUTHOR]

Excessive alcohol consumption can cause alcoholic myopathy, but the molecular mechanism is still unclear. In this study, zebrafish were exposed to 0.5% alcohol for eight weeks to investigate the effect of alcohol on skeletal muscle and its molecular mechanism. The results showed that the body length, body weight, cross-sectional area of the skeletal muscle fibers, Ucrit, and MO2max of the zebrafish were significantly decreased after alcohol exposure. The expression of markers of skeletal muscle atrophy and autophagy was increased, and the expression of P62 was significantly reduced. The content of ROS, the mRNA expression of sod1 and sod2, and the protein expression of Nox2 were significantly increased. In addition, we found that the inflammatory factors Il1β and Tnfα were significantly enriched in skeletal muscle, and the expression of the HMGB1/TLR4/NF-κB signaling axis was also significantly increased. In summary, in this study, we established a zebrafish model of alcohol-induced skeletal muscle atrophy and further elucidated its pathogenesis. [ABSTRACT FROM AUTHOR]

Previous work has demonstrated that the expression of microRNA-21 (miR-21) is implicated in cervical cancer (CC). However, little is known regarding its associations with clinical parameters. We first conducted a meta-analysis using data from Gene Expression Omnibus (GEO) microarrays and The Cancer Genome Atlas (TCGA). Then, enrichment analysis and hub gene screening were performed by bioinformatic methods. Finally, the role of the screened target genes in CC was explored. According to the meta-analysis, the expression of miR-21 in cancer tissues was higher than in adjacent nontumor tissues (P < 0.05). In addition, 46 genes were predicted as potential targets of miR-21. After enrichment analyses, it was detected that these genes were enriched in various cancer pathways, including the phosphatidylinositol signaling system and mammalian target of rapamycin (mTOR) signaling pathway. In this study, bioinformatic tools and meta-analysis validated that miR-21 may function as a highly sensitive and specific marker for the diagnosis of CC, which may provide a novel approach to the diagnosis and treatment of CC. [ABSTRACT FROM AUTHOR]

Originating in the subtropics, cucumbers require warm weather and plenty of light, low light inhibits the growth of cucumbers. For cucumbers to efficiently absorb light energy in low light, chlorophyll synthesis is necessary. Oxygenase for chlorophyllate is encoded by CsCAO. RNA interference (RNAi) was used to reduce CsCAO expression in cucumber, reduced chlorophyll b content and Fv/Fm (maximal photochemical efficiency of photosystem II) were found in RNAi- CsCAO lines. The Arabidopsis Atcao mutant lacks chlorophyll b and has a low Fv/Fm, but overexpressing CsCAO restored the mutant's phenotype. CsCAO gene expression was found to be upregulated in the presence of low light. The Y1H screening assay revealed that CsHsfA6b and CsBLH4 were potential CsCAO expression regulators. The results of the Y1H, LUC/REN, and EMSA assays confirmed that only CsBLH4 can bind to the CsCAO promoter. Furthermore, like Atcao , the Atblh4 mutant had low chlorophyll b content and Fv/Fm. CsCAO overexpression in the Atblh4 mutant increased the content of chlorophyll b and Fv/Fm, especially under low light conditions. CsBLH4 targeting CsCAO was found to positively regulate chlorophyll b synthesis and photosynthetic capacity in cucumber under low light conditions in our study. • Low light promoted the accumulation of chlorophyll b by up-regulating the transcription level of CsCAO. • It clarified the regulatory mechanism of BLH family member involved in chlorophyll b synthesis. • The synthesis of chlorophyll plays an important role in the response of cucumber to low light stress. [ABSTRACT FROM AUTHOR]

• By inhibiting SLC7A11/xCT with the inhibitor sulfasalazine and nanoreactors with tetrasulfide bond (-s-s-s-s-)- as the backbone, tumor cell glutathione synthesis is suppressed and its consumption is promoted. • Decreased glutathione content inhibits GPX4 synthesis, promotes intracellular lipid peroxide accumulation, and induces ferroptosis in tumor cells. • The photosensitizer DVDMS produces ROS under ultrasound, which, together with Fe3+, promotes lipid peroxide generation. • Targeted delivery of USP39 shRNA can efficiently silence USP39 gene expression under ultrasound stimulation, inhibiting cell proliferation and selectively inducing autophagy-dependent ferroptosis. The promotion of cellular ferroptosis through ultrasound (US)-assisted Fenton chemistry has emerged as a promising strategy for tumor therapy. To enhance the therapeutic effect, we designed a GSH-responsive ultrasound-driven nanoreactor for RNA interference (RNAi)-intensified ferroptosis in synergistic sono-chemodynamic therapy. Our nanoreactor comprises Fe3+/tetrasulfide bond (-s-s-s-s-) enriched dendritic organosilica encapsulating USP39 shRNA, along with co-loading of sinophoryrin sodium (DVDMS) and sulfasalazine (SAS). Hyaluronic acid surface functionalization ensures high tumor accumulation for active targeting of tumor cells. Upon internalization into tumor cells, the nanoreactor degrades upon the triggering of intracellular overproduced GSH. Ultrasound-triggered release of DVDMS generates large amounts of ROS, synergizing with Fe-catalyzed Fenton chemistry. The simultaneous depletion of glutathione peroxidase 4 and GSH by SAS and Fe3+ weakens the ROS-scavenging system, leading to tumoral redox dyshomeostasis via oxidative stress amplification. This results in the accumulation of lipid peroxide in tumor cells, efficiently inducing ferroptosis. Additionally, USP39 shRNA effectively silences the expression of the USP39 gene in cells, inhibiting tumor cell proliferation, while promoting ATG5 gene expression to intensify ferroptosis. Our work provides a promising nanoreactor for high-efficiency synergistic tumor therapy via RNAi-intensified ferroptosis, highlighting the potential of sono-chemodynamic therapy in cancer treatment. [ABSTRACT FROM AUTHOR]

Cucumber (Cucumis sativus L.) is a high water-demanding and drought-susceptible vegetable crop. Basic leucine zipper (bZIP) transcription factors (TFs) have been linked to drought stress response in plants. Here we characterized a G subfamily gene in cucumber, CsbZIP50 , which was strongly induced by drought stress and an exogenous abscisic acid (ABA) treatment. Under drought stress, CsbZIP50 -overexpressing plants exhibited enhanced drought tolerance compared with wild-type plants, as indicated by the higher antioxidant enzyme activities but lower reactive oxygen species (ROS) and malondialdehyde contents. In addition, overexpression of CsbZIP50 enhanced cucumber's sensitivity to exogenously applied ABA, and up-regulated the expression of its stress-related genes. Moreover, we found that CsbZIP50 activated CsRD29 expression by directly binding to the G-box/ABRE cis-acting element in its promoter, both in vitro and in vivo. Yeast two-hybrid, luciferase complementation imaging, and pull-down assays showed that CsbZIP50 physically interacted with two IQ domain-containing proteins, CsIQD1 and CsIQD4, both of which promoted the ability of CsbZIP50 to activate the expression of CsRD29. Taken together, our results show that CsbZIP50 enhances drought stress tolerance in cucumber by regulating drought-responsive gene expression and ROS levels. • CsbZIP50 is a G subfamily of the bZIP TF, which was induced by drought stress and exogenous ABA treatment. • Expression of CsbZIP50 positively regulates drought tolerance by improving stomata closure and ROS scavenging. • CsbZIP50 targeted CsRD29A and the expression activation effect was enhanced by interacting with CsIQD1 and CsIQD4. [ABSTRACT FROM AUTHOR]