The role of exogenous hydrogen sulfide in mitigating cadmium toxicity in plants: A comprehensive meta-analysis.

Reducing the accumulation of cadmium (Cd) and mitigating its toxicity are pivotal strategies for addressing Cd pollution's threats to agriculture and human health. Hydrogen sulfide (H2S) serves as a signaling molecule, playing a crucial role in plant stress defense mechanisms. Nevertheless, a comprehensive assessment of the impact of exogenous H2S on plant growth, antioxidant properties, and gene expression under Cd stress remains lacking. In this meta-analysis, we synthesized 575 observations from 27 articles, revealing that exogenous H2S significantly alleviates Cd-induced growth inhibition in plants. Specifically, it enhances root length (by 8.71%), plant height (by 15.67%), fresh weight (by 15.15%), dry weight (by 22.54%), and chlorophyll content (by 27.99%) under Cd stress conditions. H2S boosts antioxidant enzyme activity, particularly catalase (CAT), by 39.51%, thereby reducing Cd-induced reactive oxygen species (ROS) accumulation. Moreover, it impedes Cd translocation from roots to shoots, resulting in a substantial 40.19% reduction in stem Cd content. Additionally, H2S influences gene expression in pathways associated with antioxidant enzymes, metal transport, heavy metal tolerance, H2S biosynthesis, and energy metabolism. However, the efficacy of exogenous H2S in alleviating Cd toxicity varies depending on factors such as plant species, concentration of the H2S donor sodium hydrosulfide (NaHS), application method, and cultivation techniques. Notably, NaHS concentrations exceeding 200 µM may adversely affect plants. Overall, our study underscores the role of exogenous H2S in mitigating Cd toxicity and elucidates its mechanism, providing insights for utilizing H2S to combat Cd pollution in agriculture.

Overexpression of SQUAMOSA promoter binding protein-like 4a (NtSPL4a) alleviates Cd toxicity in Nicotiana tabacum.

Squamosa Promoter Binding Protein-Like (SPL) plays a crucial role in regulating plant development and combating stress, yet its mechanism in regulating resistance to Cd toxicity remains unclear. In this study, we cloned a nuclear-localized transcription factor, NtSPL4a, from the tobacco cultivar TN90. Transient co-expression results showed that miR156 significantly reduced the expression of NtSPL4a by binding to the 3'-UTR of its transcript. We obtained transgenic tobacco overexpressing NtSPL4a (including the 3'-UTR) and NtSPL4aΔ (lacking the 3'-UTR) through Agrobacterium-mediated genetic transformation. Compared to the wild type (WT), overexpression of NtSPL4a/NtSPL4aΔ shortened the flowering time and exhibited a more developed root system. The transgenic tobacco showed significantly reduced Cd content, being 85.1% (OE-NtSPL4a) and 46.7% (OE-NtSPL4aΔ) of WT, respectively. Moreover, the upregulation of NtSPL4a affected the mineral nutrient homeostasis in transgenic tobacco. Additionally, overexpression of NtSPL4a/NtSPL4aΔ effectively alleviated leaf chlorosis and oxidative stress induced by Cd toxicity. One possible reason is that the overexpression of NtSPL4a/NtSPL4aΔ can effectively promote the accumulation of non-enzymatic antioxidants. A comparative transcriptomic analysis was performed between transgenic tobacco and WT to further unravel the global impacts brought by NtSPL4a. The tobacco overexpressing NtSPL4a had 183 differentially expressed genes (77 upregulated, 106 downregulated), while the tobacco overexpressing NtSPL4aΔ had 594 differentially expressed genes (244 upregulated, 350 downregulated) compared to WT. These differentially expressed genes mainly included transcription factors, metal transport proteins, flavonoid biosynthesis pathway genes, and plant stress-related genes. Our study provides new insights into the role of the transcript factor SPL in regulating Cd tolerance.

Overexpression of NtGPX8a Improved Cadmium Accumulation and Tolerance in Tobacco (Nicotiana tabacum L.).

Cadmium (Cd)-induced oxidative stress detrimentally affects hyperaccumulator growth, thereby diminishing the efficacy of phytoremediation technology aimed at Cd pollution abatement. In the domain of plant antioxidant mechanisms, the role of glutathione peroxidase (GPX) in conferring Cd tolerance to tobacco (Nicotiana tabacum) remained unclear. Our investigation employed genome-wide analysis to identify 14 NtGPX genes in tobacco, revealing their organization into seven subgroups characterized by analogous conserved domain patterns. Notably, qPCR analysis highlighted NtGPX8a as markedly responsive to Cd2+ stress. Subsequent exploration through yeast two-hybridization unveiled NtGPX8a's utilization of thioredoxins AtTrxZ and AtTrxm2 as electron donors, and without interaction with AtTrx5. Introduction of NtGPX8a into Escherichia coli significantly ameliorated Cd-induced adverse effects on bacterial growth. Transgenic tobacco overexpressing NtGPX8a demonstrated significantly augmented activities of GPX, SOD, POD, and CAT under Cd2+ stress compared to the wild type (WT). Conversely, these transgenic plants exhibited markedly reduced levels of MDA, H2O2, and proline. Intriguingly, the expression of NtGPX8a in both E. coli and transgenic tobacco led to increased Cd accumulation, confirming its dual role in enhancing Cd tolerance and accumulation. Consequently, NtGPX8a emerges as a promising candidate gene for engineering transgenic hyperaccumulators endowed with robust tolerance for Cd-contaminated phytoremediation.

The transcription factor PtoMYB142 enhances drought tolerance in Populus tomentosa by regulating gibberellin catabolism.

Drought stress caused by global warming has resulted in significant tree mortality, driving the evolution of water conservation strategies in trees. Although phytohormones have been implicated in morphological adaptations to water deficits, the molecular mechanisms underlying these processes in woody plants remain unclear. Here, we report that overexpression of PtoMYB142 in Populus tomentosa results in a dwarfism phenotype with reduced leaf cell size, vessel lumen area, and vessel density in the stem xylem, leading to significantly enhanced drought resistance. We found that PtoMYB142 modulates gibberellin catabolism in response to drought stress by binding directly to the promoter of PtoGA2ox4, a GA2-oxidase gene induced under drought stress. Conversely, knockout of PtoMYB142 by the CRISPR/Cas9 system reduced drought resistance. Our results show that the reduced leaf size and vessel area, as well as the increased vessel density, improve leaf relative water content and stem water potential under drought stress. Furthermore, exogenous GA3 application rescued GA-deficient phenotypes in PtoMYB142-overexpressing plants and reversed their drought resistance. By suppressing the expression of PtoGA2ox4, the manifestation of GA-deficient characteristics, as well as the conferred resistance to drought in PtoMYB142-overexpressing poplars, was impeded. Our study provides insights into the molecular mechanisms underlying tree drought resistance, potentially offering novel transgenic strategies to enhance tree resistance to drought.

The Roles and Regulation of Ferroptosis in Cancer Progression.

Ferroptosis is an iron-dependent, nonapoptotic form of regulatory death and has received extensive attention. Fenton reaction related to iron metabolism release high levels of Reactive Oxygen Species (ROS), and the intracellular ROS content is closely related to various diseases; the iron ion concentration in many diseased cells is also disordered. In this paper, the advances in ferroptosis research are summarized, and the regulatory mechanisms of ferroptosis, including inducers and regulatory protein of ferroptosis in cancer progression. We expect that this study will benefit the further development of basic research and clinical application of ferroptosis for cancer treatment.

TRAF4 Promotes the Proliferation of Glioblastoma by Stabilizing SETDB1 to Activate the AKT Pathway.

The process of ubiquitination regulates the degradation, transport, interaction, and stabilization of substrate proteins, and is crucial for cell signal transduction and function. TNF receptor-associated factor 4, TRAF4, is a member of the TRAF family and is involved in the process of ubiquitination as an E3 ubiquitin protein ligase. Here, we found that TRAF4 expression correlates with glioma subtype and grade, and that TRAF4 is significantly overexpressed in glioblastoma and predicts poor prognosis. Knockdown of TRAF4 significantly inhibited the growth, proliferation, migration, and invasion of glioblastoma cells. Mechanistically, we found that TRAF4 only interacts with the Tudor domain of the AKT pathway activator SETDB1. TRAF4 mediates the atypical ubiquitination of SETDB1 to maintain its stability and function, thereby promoting the activation of the AKT pathway. Restoring SETDB1 expression in TRAF4 knockdown glioblastoma cells partially restored cell growth and proliferation. Collectively, our findings reveal a novel mechanism by which TRAF4 mediates AKT pathway activation, suggesting that TRAF4 may serve as a biomarker and promising therapeutic target for glioblastoma.

The Superoxide Dismutase Gene Family in Nicotiana tabacum: Genome-Wide Identification, Characterization, Expression Profiling and Functional Analysis in Response to Heavy Metal Stress.

Superoxide dismutases (SODs) play an important role in protecting plants against ROS toxicity induced by biotic and abiotic stress. Recent studies have shown that the SOD gene family is involved in plant growth and development; however, knowledge of the SOD gene family in tobacco is still limited. In the present study, the SOD gene family was systematically characterized in the tobacco genome. Based on the conserved motif and phylogenetic tree, 15 NtSOD genes were identified and classified into three subgroups, including 5 NtCSDs, 7 NtFSDs and 3 NtMSDs. The predicted results of the transport peptide or signal peptide were consistent with their subcellular localization. Most NtSOD genes showed relatively well-maintained exon-intron and motif structures in the same subgroup. An analysis of cis-acting elements in SOD gene promoters showed that NtSOD expression was regulated by plant hormones, defense and stress responses, and light. In addition, multiple transcription factors and miRNAs are predicted to be involved in the regulation of NtSOD gene expression. The qPCR results indicated specific spatial and temporal expression patterns of the NtSOD gene family in different tissues and developmental stages, and this gene family played an important role in protecting against heavy metal stress. The results of functional complementation tests in the yeast mutant suggested that NtCSD1a, NtFSD1e and NtMSD1b scavenge ROS produced by heavy metal stress. This study represents the first genome-wide analysis of the NtSOD gene family, which lays a foundation for a better understanding of the function of the NtSOD gene family and improving the tolerance of plants to heavy metal toxicity.

Regulation of Glucose, Fatty Acid and Amino Acid Metabolism by Ubiquitination and SUMOylation for Cancer Progression.

Ubiquitination and SUMOylation, which are posttranslational modifications, play prominent roles in regulating both protein expression and function in cells, as well as various cellular signal transduction pathways. Metabolic reprogramming often occurs in various diseases, especially cancer, which has become a new entry point for understanding cancer mechanisms and developing treatment methods. Ubiquitination or SUMOylation of protein substrates determines the fate of modified proteins. Through accurate and timely degradation and stabilization of the substrate, ubiquitination and SUMOylation widely control various crucial pathways and different proteins involved in cancer metabolic reprogramming. An understanding of the regulatory mechanisms of ubiquitination and SUMOylation of cell proteins may help us elucidate the molecular mechanism underlying cancer development and provide an important theory for new treatments. In this review, we summarize the processes of ubiquitination and SUMOylation and discuss how ubiquitination and SUMOylation affect cancer metabolism by regulating the key enzymes in the metabolic pathway, including glucose, lipid and amino acid metabolism, to finally reshape cancer metabolism.

Therapeutic targeting of both dihydroorotate dehydrogenase and nucleoside transport in MYCN-amplified neuroblastoma.

Metabolic reprogramming is an integral part of the growth-promoting program driven by the MYC family of oncogenes. However, this reprogramming also imposes metabolic dependencies that could be exploited therapeutically. Here we report that the pyrimidine biosynthetic enzyme dihydroorotate dehydrogenase (DHODH) is an attractive therapeutic target for MYCN-amplified neuroblastoma, a childhood cancer with poor prognosis. Gene expression profiling and metabolomic analysis reveal that MYCN promotes pyrimidine nucleotide production by transcriptional upregulation of DHODH and other enzymes of the pyrimidine-synthesis pathway. Genetic and pharmacological inhibition of DHODH suppresses the proliferation and tumorigenicity of MYCN-amplified neuroblastoma cell lines. Furthermore, we obtain evidence suggesting that serum uridine is a key factor in determining the efficacy of therapeutic agents that target DHODH. In the presence of physiological concentrations of uridine, neuroblastoma cell lines are highly resistant to DHODH inhibition. This uridine-dependent resistance to DHODH inhibitors can be abrogated by dipyridamole, an FDA-approved drug that blocks nucleoside transport. Importantly, dipyridamole synergizes with DHODH inhibition to suppress neuroblastoma growth in animal models. These findings suggest that a combination of targeting DHODH and nucleoside transport is a promising strategy to overcome intrinsic resistance to DHODH-based cancer therapeutics.

Ferroptosis: A Novel Mechanism of Artemisinin and its Derivatives in Cancer Therapy.

BACKGROUND: Artemisinin is a sesquiterpene lactone compound with a special peroxide bridge that is tightly linked to the cytotoxicity involved in fighting malaria and cancer. Artemisinin and its derivatives (ARTs) are considered to be potential anticancer drugs that promote cancer cell apoptosis, induce cell cycle arrest and autophagy, inhibit cancer cell invasion and migration. Additionally, ARTs significantly increase intracellular Reactive Oxygen Species (ROS) in cancer cells, which result in ferroptosis, a new form of cell death, depending on the ferritin concentration. Ferroptosis is regarded as a cancer suppressor and as well as considered a new mechanism for cancer therapy. METHODS: The anticancer activities of ARTs and reference molecules were compared by literature search and analysis. The latest research progress on ferroptosis was described, with a special focus on the molecular mechanism of artemisinin-induced ferroptosis. RESULTS: Artemisinin derivatives, artemisinin-derived dimers, hybrids and artemisinin-transferrin conjugates, could significantly improve anticancer activity, and their IC50 values are lower than those of reference molecules such as doxorubicin and paclitaxel. The biological activities of linkers in dimers and hybrids are important in the drug design processes. ARTs induce ferroptosis mainly by triggering intracellular ROS production, promoting the lysosomal degradation of ferritin and regulating the System Xc-/Gpx4 axis. Interestingly, ARTs also stimulate the feedback inhibition pathway. CONCLUSION: Artemisinin and its derivatives could be used in the future as cancer therapies with broader applications due to their induction of ferroptosis. Meanwhile, more attention should be paid to the development of novel artemisinin-related drugs based on the mechanism of artemisinininduced ferroptosis.

Deficiency of microRNA-628-5p promotes the progression of gastric cancer by upregulating PIN1.

Gastric cancer is one of the most common cancer and is the second leading cause of cancer-related mortality in the world. PIN1, belonging to peptidyl-prolyl cis-trans isomerase family, uniquely catalyzes the structural transformation of phosphorylated Ser/Thr-Pro motif. It's high expressed in most cancers and promotes their progression. However, the mechanism of PIN1 high expression and its function in gastric cancer progression are still unclear. In this research, we revealed that PIN1 not only promotes the proliferation and colony formation of gastric cancer, but also increases its migration and invasion. The PIN1 expression in metastasis lesion is usually higher than the corresponding primary site. Inhibiting PIN1 by shRNA suppresses the progression of gastric cancer significantly. Besides, we demonstrated that miR-628-5p is a novel PIN1-targeted microRNA, and the expression of miR-628-5p is negatively correlated with PIN1 in gastric cancer. Exogenous expression of miR-628-5p inhibits the progression of gastric cancer that revered by restoring PIN1 expression. However, miR-628-5p is downregulated in majority of gastric cancer tissue especially in metastasis lesion. The lower miR-628-5p level indicates poorer prognosis. In summary, our study demonstrated that deficient miR-628-5p expression facilitates the expression of PIN1, and consequently promotes the progression of gastric cancer.

Histone Deacetylase Inhibitor Trichostatin A Suppresses Cell Proliferation and Induces Apoptosis by Regulating the PI3K/AKT Signalling Pathway in Gastric Cancer Cells.

BACKGROUND: Gastric cancer, a common malignant tumour worldwide, has a relatively poor prognosis and is a serious threat to human health. Histone Deacetylase Inhibitors (HDACi) are anticancer agents that are known to affect the cell growth of different cancer types. Trichostatin A (TSA) selectively inhibits the class I and II mammalian Histone Deacetylase (HDAC) family enzymes and regulates many cell processes. Still, the underlying mechanisms of HDACs are not fully understood in gastric cancer. OBJECTIVE: This study aims to investigate the antitumor effect and the mechanism of growth modulation of gastric cancer cells by TSA. METHODS: The cell proliferation of gastric cancer cells was measured by MTT and BrdU immunofluorescence assays. Soft agar assay was used to detect the colony formation ability of gastric cancer cells. Flow cytometry was used to examine cell cycle and apoptosis. Western blot was employed to detect protein expression of target factors. RESULTS: TSA inhibits the proliferation of MKN-45 and SGC-7901 cells and leads to significant repression of colony number and size. Flow cytometry assays show TSA induces cell cycle arrest at G1 phase and apoptosis, and TSA effects the expression of related factors in the mitochondrial apoptotic signalling and cell cycle-related regulatory pathways. Furthermore, TSA increased histone H3K27 acetylation and downregulated the expression of PI3K and p-AKT. CONCLUSION: Downregulating PI3K/AKT pathway activation is involved in TSA-mediated proliferation inhibition of gastric cancer.

[Function of histone demethylasehistone lysine-specific demethylase 1A in tumor initiation and progression].

As a member of the histone lysine-specific demethylase family, KDM1A plays a pivotal role in biological processes including signal transduction, chromatin reprogramming, embryo development, hematopoiesis, glucose and lipid metabolism. Recently, increasing studies and clinical evidences suggest that the expression of KDM1A is related to initiation and development of tumors and plays a key role in regulating of initiation and development of tumors, such as prostate cancer, breast cancer, lung cancer and liver cancer. KDM1A binds to distinct complexes and mediates different downstream signaling pathways. However, KDM1A often plays an oncogenic role in the initiation and development of tumors. Based on the current literatures, we describe the latest research of KDM1A in the initiation and progression of various tumors, and summarize its mechanism of actions, to provide clues for cancer therapy.

Hedgehog promotes cell proliferation in the midgut of silkworm, Bombyx mori.

The Hedgehog (Hh) signaling pathway is one of the major regulators of embryonic development and tissue homeostasis in multicellular organisms. However, the role of this pathway in the silkworm, especially in the silkworm midgut, remains poorly understood. Here, we report that Bombyx mori Hedgehog (BmHh) is expressed in most tissues of silkworm larvae and that its functions are well-conserved throughout evolution. We further demonstrate that the messenger RNA of four Hh signaling components, BmHh ligand, BmPtch receptor, signal transducer BmSmo and transcription factor BmCi, are all upregulated following Escherichia coli or Bacillus thuringiensis infection, indicating the activation of the Hh pathway. Simultaneously, midgut cell proliferation is strongly promoted. Conversely, the repression of Hh signal transduction with double-stranded RNA or cyclopamine inhibits the expression of BmHh and BmCi and reduces cell proliferation. Overall, these findings provide new insights into the Hh signaling pathway in the silkworm, B. mori.

Down-Regulation of Phosphoribosyl Pyrophosphate Synthetase 1 Inhibits Neuroblastoma Cell Proliferation.

Phosphoribosyl pyrophosphate synthetase 1 (PRPS1) is a key enzyme in de novo nucleotide synthesis and nucleotide salvage synthesis pathways that are critical for purine and pyrimidine biosynthesis. Abnormally high expression of PRPS1 can cause many diseases, including hearing loss, hypotonia, and ataxia, in addition to being associated with neuroblastoma. However, the role of PRPS1 in neuroblastoma is still unclear. In this study, we found that PRPS1 was commonly expressed in neuroblastoma cells and was closely related to poor prognosis for cancer. Furthermore, down-regulation of PRPS1 inhibited neuroblastoma cell proliferation and tumor growth in vitro and in vivo via disturbing DNA synthesis. This study provides new insights into the treatment of neuroblastoma patients and new targets for drug development.

BMP4 and Neuregulin regulate the direction of mouse neural crest cell differentiation.

The neural crest is a transient embryonic tissue that initially generates neural crest stem cells, which then migrate throughout the body to give rise to a variety of mature tissues. It was proposed that the fate of neural crest cells is gradually determined via environmental cues from the surrounding tissues. In the present study, neural crest cells were isolated and identified from mouse embryos. Bone morphogenetic protein 4 (BMP4) and Neuregulin (NRG) were employed to induce the differentiation of neural crest cells. Treatment with BMP4 revealed neuron-associated differentiation; cells treated with NRG exhibited differentiation into the Schwann cell lineage, a type of glia. Soft agar clonogenic and neurosphere formation assays were conducted to investigate the effects of N-Myc (MYCN) overexpression in neural crest cells; the number of colonies and neurospheres notably increased after 14 days. These findings demonstrated that the direction of cell differentiation may be affected by altering the factors present in the surrounding environment. In addition, MYCN may serve a key role in regulating neural crest cell differentiation.

Correction: Inhibition of H3K9 Methyltransferase G9a Repressed Cell Proliferation and Induced Autophagy in Neuroblastoma Cells.

[This corrects the article DOI: 10.1371/journal.pone.0106962.].

The roles of sirtuins family in cell metabolism during tumor development.

Altering energy metabolism to meet the uncontrolled proliferation and metastasis has emerged as one of the most significant hallmarks in tumors. However, the detailed molecular mechanisms and regulatory actions underlying have not been fully elucidated. As a family of NAD+ dependent protein modifying enzymes, sirtuins (SIRT1-SIRT7) have multiple catalytic functions such as deacetylase, desuccinylase, demalonylase, demyristoylase, depalmitoylase, and/or mono-ADP-ribosyltransferase. They play important roles in regulating cell metabolism, especially in glucose and lipid metabolism, thereby exerting complex functions in either increasing or decreasing malignant characteristics in tumors. This review highlights the major function and its mechanisms of sirtuins in cellular metabolic reprogramming, such as glucose metabolism including aerobic glycolysis (the Warburg effect), oxidative phosphorylation (OXPHOS)/tricarboxylic acid (TCA) cycle and glutamine metabolism; lipometabolism including fatty acid metabolism, cholesterol metabolism, ketone body metabolism and acetate metabolism; as well as leucine metabolism and the urea cycle in tumorigenesis and cancer development.

Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway.

It is generally known that glioblastoma is the most common primary malignant brain tumor and that it is highly aggressive and deadly. Although surgical and pharmacological therapies have made long­term progress, glioblastoma remains extremely lethal and has an uncommonly low survival rate. Therefore, further elucidation of the molecular mechanisms of glioblastoma initiation and its pathological processes are urgent. Arsenic resistance protein 2 (Ars2) is a highly conserved gene, and it has been found to play an important role in microRNA biosynthesis and cell proliferation in recent years. Furthermore, absence of Ars2 results in developmental death in Drosophila, zebrafish and mice. However, there are few studies on the role of Ars2 in regulating tumor development, and the mechanism of its action is mostly unknown. In the present study, we revealed that Ars2 is involved in glioblastoma proliferation and we identified a potential mechanistic role for it in cell cycle control. Our data demonstrated that Ars2 knockdown significantly repressed the proliferation and tumorigenesis abilities of glioblastoma cells in vitro and in vivo. Further investigation clarified that Ars2 deficiency inhibited the activation of the MAPK/ERK pathway, leading to cell cycle arrest in the G1 phase, resulting in suppression of cell proliferation. These findings support the conclusion that Ars2 is a key regulator of glioblastoma progression.

Demethylzeylasteral inhibits glioma growth by regulating the miR-30e-5p/MYBL2 axis.

Glioma is the most common and malignant form of primary brain tumour, and is characterised by high proliferation and extensive invasion and neurological destruction. Demethylzeylasteral (T-96), which is extracted from Tripterygium wilfordii, is considered to have immunosuppressive, anti-inflammatory and anti-angiogenic effects. Here, the anti-tumour effect of T-96 on glioma was evaluated. Our results demonstrated that T-96 significantly inhibited glioma cell growth and induced cell cycle arrest in G1 phase but did not induce apoptosis. Cell invasion and migration were dramatically suppressed after treatment with T-96. Almost all genes related to cell cycle and DNA replication were downregulated after treatment with T-96. Our results showed that miR-30e-5p was noticeably upregulated after T-96 treatment, and MYBL2, which is involved in cell cycle progression and is a target gene of miR-30e-5p, was significantly reduced in synchrony. Overexpression of MYBL2 partially rescued the T-96-induced inhibition of cell growth and proliferation. Moreover, a miR-30e-5p antagomir significantly reduced the upregulation of miR-30e-5p expression induced by T-96, leading to recovery of MYBL2 expression, and partially rescued the T-96-induced inhibition of cell growth and proliferation. More important, T-96 effectively upregulated miR-30e-5p expression and downregulated MYBL2 expression, thus inhibiting LN-229 cell tumour growth in a mouse model. These results indicated that T-96 might inhibit glioma cell growth by regulating the miR-30e-5p/MYBL2 axis. Our study demonstrated that T-96 might act as a promising agent for malignant glioma therapy.