syedzayyan/paper_mill_benchmark huggingface dataset:
Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

Spinal cord glioma is a highly aggressive malignancy that commonly results in high mortality due to metastasis, high recurrence and limited treatment regimens.This study aims to elucidate the effects of long non-coding rna linc01260 (linc01260) on the proliferation, migration and invasion of spinal cord glioma cells by targeting caspase recruitment domain family, member 11 (card11) via nuclear factor kappa b (nf-κb) signaling.Methods: the multi experiment matrix (mem) website was used for target gene prediction, and the david database was used for analysis of the relationship between card11 and the nf-κb pathway.In total, 60 cases of glioma tissues and adjacent normal tissues were collected.Human u251 glioma cells were grouped into blank, negative control (nc), linc01260 vector, card11 vector, si rna-linc01260, si rna-card11, linc01260 vector + card11 vector and linc01260 + si rna-card11 groups.A dual-luciferase reporter assay was conducted to verify the target relationship between linc01260 and card11.Reverse transcription quantitative polymerase chain reaction (rt-q pcr) and western blot analysis were employed to assess expression of linc01260, e-cadherin, p53, card11, ki67, n-cadherin, matrix metalloproteinase (mmp)-9, nf-κbp65 and nf-κbp50.Mtt, flow cytometry, wound-healing and transwell assays were performed to examine cell viability, the cell cycle, apoptosis, invasion and migration.Tumor growth was assessed through xenografts in nude mice.Results: card11 was confirmed to be a target gene of linc01260 and was found to be involved in regulating the nf-κb pathway.Compared with adjacent normal tissues, glioma tissues showed reduced expression of linc01260 and elevated expression of card11 and genes related to apoptosis, invasion and migration; activation of nf-κb signaling was also observed.In contrast to the blank and nc groups, an elevated number of cells arrested in g1 phase, increased apoptosis and reduced cell proliferation, invasion and number of cells arrested in s and g2 phases, as well as tumor growth were found for the linc01260 vector and si rna-card11 groups.Conclusions: our findings demonstrate that overexpression of linc01260 inhibits spinal cord glioma cell proliferation, migration and invasion by targeting card11 via nf-κb signaling suppression.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Downregulation of NGAL is Required for the Inhibition of Proliferation and the Promotion of Apoptosis of Human Gastric Cancer MGC-803 Cells

Gastric cancer is considered as a common malignancy with a poor prognosis as well as unsatisfactory treatment.Neutrophil gelatinase-associated lipocalin (ngal) has been reported to affect multiple aspects of human tumor, including gastric cancer.This study aims to explore the effects of ngal gene silencing on the proliferation as well as apoptosis of human gastric cancer mgc-803 cells.Methods: this study included 87 patients with gastric cancer.Mgc-803 cells were collected and mainly treated with si rna against ngal and recombinant ngal plasmid.The expression of ngal m rna and the expressions of ngal protein and apoptosis-related proteins were determined by reverse transcription-quantitative polymerase chain reaction (rt-q pcr) and western blot analysis, respectively.Cell cycle and apoptosis were tested by flow cytometry, and cell proliferation was detected by water soluble tetrazolium-1 (wst-1) assay.The effect of ngal gene silencing on tumorigenicity of mgc-803 cells in vivo was detected through establishment of xenograft in nude mice.Results: ngal was highly expressed in gastric cancer tissues.The protein and m rna expressions of ngal gene in mgc-803 cells treated with ngal-si rna were obviously reduced, and the amount of cells in g0/g1 phase was increased.Moreover, mgc-803 cells treated with ngal-si rna exhibited inhibited proliferation, enhanced apoptosis, decreased expressions of nuclear factor kappa-light-chain-enhancer of activated b cells (nf-κb) as well as b-cell lymphoma-2 (bcl-2) and increased expressions of cysteine-aspartic acid specific protease-9 (caspase-9) and bcl2-associated x (bax), as well as repressed tumorigenicity in vivo.Conclusion: ngal gene silencing inhibits proliferation and promotes apoptosis of mgc-803 cells, which can provide a novel theory for treatment of gastric cancer.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Inhibition of microRNA-200a Upregulates the Expression of Striatal Dopamine Receptor D2 to Repress Apoptosis of Striatum via the cAMP/PKA Signaling Pathway in Rats with Parkinson’s Disease

Parkinson’s disease (pd) is a neurodegenerative movement disease with a high annual incidence.Accumulating evidence demonstrates that micro rnas play important roles in the pathogenesis of multiple neurological disorders, including pd.This study aims to investigate how micro rna-200a (mi r-200a) regulates striatal dopamine receptor d2 (drd2) to affect apoptosis of striatum in rats with pd and to explore the associated mechanism.Methods: after successfully establishing a pd model by 6-hydroxydopamine injections, pd rats were mainly treated with mi r-200a mimics, inhibitors, forskolin or a combination of mi r-200a inhibitors and forskolin.High-performance liquid chromatography-electrochemical detection (hplc-ecd) was employed to detect the levels of dopamine, 3, 4-dihydroxyphenylacetic acid (dopac) and homovanillic acid (hva), and chemistry colorimetric methods were applied to detect the levels of malondialdehyde (mda), superoxide dismutase (sod) and glutathione peroxidase (gsh-px).A tunel assay and immunocytochemical staining were performed to observe apoptosis and tyrosine hydroxylase (th)-positive cells in the striatum.The expression of mi r-200a, drd2, bad, bax, bcl-2, c amp and pka was determined by reverse transcription quantitative polymerase chain reaction (rt-q pcr) and western blot assays.Results: in the cellular experiments, after transfection with the inhibitor of mi r-200a, decreased levels of bax, gsh-px, sod, dopamine, dopac and hva but increased levels of mda and bcl-2 were found along with a reduced apoptosis rate and increased th-positive cell number.In addition, downregulating mi r-200a resulted in lower expression of akt, c amp and pka but higher expression of drd2 and creb, indicating that the downregulation of mi r-200a increases drd2 expression, which blocks the c amp/pka signaling pathway.Conclusion: this study provides evidence that the inhibition of mi r-200a can repress apoptosis in the striatum via inhibition of the c amp/pka signaling pathway by upregulating drd2 expression in pd rats.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Numerous studies have highlighted the activation of nf-κb in the esophageal mucosa during the early stages of gastroesophageal reflux disease (gerd).The present study aimed to investigate the role of the tlr4/nf-κb signaling pathway in gerd rat models.Methods: wistar rats (n = 60) were recruited to establish a gerd animal model.Distal esophageal p h was assessed, followed by determination of the contents of thiobarbituric acid-reactive species (tbars) and reactive oxygen species (ros) in esophageal mucosa homogenate.Elisa was employed to detect the levels of inflammatory factors (il-6, il-8, il-10 and tnf-α) in esophageal mucosa.The expression of mmp-3, mpp-9, cldn1 and cldn4 was determined by immunohistochemistry.Rt-q pcr and western blot analysis were applied to evaluate the protein expressions in tlr4/nf-κb signaling pathway, while tunel staining was utilized to examine the apoptosis rate in the esophageal mucosal tissues.Results: distal esophageal p h of the rats was higher in the gerd + pdtc group than in other groups.Levels of inflammatory factors in esophageal mucosal tissues were downregulated with the inhibition of nf-κb, which was determined to be associated with the decreased contents of tbars and ros.Moreover, decreased mmp-3 and mpp-9 in addition to elevated cldn1 and cldn4 were detected in the esophageal mucosa as a result of the inactivation of nf-κb.The tlr4/nf-κb signaling pathway-related proteins (tlr4, nf-κb and iκbα); the rate of apoptosis was demonstrated to be suppressed in the gerd + pdtc group, while inactivating nf-κb was found to alleviate the tissue damage observed in the esophageal mucosa.Conclusion: the key findings of the current study demonstrate that the inactivation of the tlr4/nf-κb signaling pathway alleviates oxidative stress injury and promotes the repair of esophageal mucosal injury among rats with gerd, highlighting a potential novel gerd mechanism.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MiR-93 blocks cell cycle progression and promotes apoptosis in uterine leiomyoma cells by targeting CCND1

Uterine leiomyoma (ul) is the most common type of benign tumor in the women's reproductive system.A number of genes has been found to play an important role in the initiation and progression of ul, including mi rnas.In this study, our results exhibited that mi r‐93, a member of mir‐106b‐25 cluster, significantly reduced the cell viability, promoted cell cycle arrest, caused apoptosis, and inhibited migration in ul cells ( p &lt; .01).Moreover, our results have provided experimental evidence that mi r‐93 regulated the biological functions of ul cells by targeting ccnd1.

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2019)
Publication types: Research Article;
The lncRNA SNHG3 accelerates papillary thyroid carcinoma progression via the miR-214-3p/PSMD10 axis

Small nucleolar rna host gene 3 (snhg3) is a long noncoding rna (lnc rna), which is known to promote oncogenesis in many cancers but its role in human papillary thyroid carcinoma (ptc) remains poorly understood.We therefore assessed snhg3 expression in ptc tissues via quantitative reverse transcription polymerase chain reaction.We additionally knocked down snhg3 in ptc cells using short‐hairpin rnas (sh rnas) to explore its functional roles in ptc.The ability of snhg3 to bind to specific micro rnas (mi rnas) was predicted using a bioinformatics tool, and this binding was confirmed via dual‐luciferase reporter and rna immunoprecipitation (rip) assays.We then used a tumor xenograft model to assess the relevance of snhg3 in vivo.We determined snhg3 expression to be elevated in ptc tissues relative to controls, with advanced tumor‐node‐metastasis stage and lymph node metastasis being associated with this expression.Knocking down snhg3 significantly reduced in vitro ptc cell migration, invasion, proliferation, and colony formation, and it further slowed the growth of tumors in vivo.We found that snhg3 could bind to mi r‐214‐3p as a competing endogenous rna (ce rna) for this mi rna, thereby regulating proteasome 26s subunit non‐atpase 10 (psmd10) expression, a mi r‐214‐3p target.These results thus indicate that snhg3 is an oncogenic lnc rna in ptc, acting at least in part via the mi r‐214‐3p/psmd10 axis.

Journal: Journal of Cellular Physiology (2020)
Publication types: Research Article;
The inhibition of tumor protein p53 by microrna-151a-3p induced cell proliferation, migration and invasion in nasopharyngeal carcinoma

A close relation between micro rna-151a-3p (mi r-151a-3p) and nasopharyngeal carcinoma (npc) has been reported, however, the molecular mechanism is still unclear.The aim of the present study was to explore the mechanism in the promotion of mi r-151a-3p to npc progression.The levels of mi r-151-3p in several npc cell lines were detected in order to screen an experimental cell line.Mi r-151a-3p mimic and inhibitor were constructed and transfected into 5-8f cells and cell proliferation were detected by cell counting kit-8 (cck-8).The apoptosis rate, cell migration and invasion were determined by flow cytometry, wound healing and transwell assays.The predicted target was further verified by luciferase reporter assay.Real-time quantification-pcr and western blot were carried out for m rna and protein level analysis.Tumor protein p53 was co-transfected to verify the functions of mi r-151a-3p.The mi r-151a-3p level in npc tissues was much higher than that in adjacent tissues.After transfecting cells with mi r-151a-3p mimic, the cell proliferation and patients’ survival rate were much increased, and this was accompanied by the increase in b-cell lymphoma 2 (bcl-2) and decreases in bax and cleaved caspase-3 (p&amp;lt;0.01).Moreover, the migration rate and number of invaded cells were also remarkably increased, however, the mi r-151a-3p inhibitor had opposite effects on the 5-8f cells.Noticeably, p53 was revealed as a potential target of mi r-151a-3p.Co-transfection of p53 could partially reverse the promotive effects of mi r-151a-3p on npc cell progression.Our data indicated that blocking p53 expression and mediated signal pathways contribute to the positive effects of mi r-151a-3p on npc cell proliferation, migration and invasion.

Journal: Bioscience Reports (2019)
Publication types: Research Article;
Resibufogenin suppresses growth and metastasis through inducing caspase-1-dependent pyroptosis via ROS-mediated NF-κB suppression in non-small cell lung cancer

The purpose of this study is to explore the antitumor properties of resibufogenin (rb) in non‐small cell lung cancer (nsclc) and elucidate its underlying mechanism.A549 and h520 cells were treated with various concentrations of rb with or without nlrp3 inhibitor (mcc950), caspase‐1 inhibitor (vx765), or n ‐acetyl‐ l ‐cysteine (an ros scavenger).Cell counting kit‐8 and colony formation assays were conducted to determine cell viability.Cell invasion was detected by using the transwell assay.The release of lactate dehydrogenase (ldh) was determined by the ldh detection assay.The protein expression levels of related genes were measured by western blotting and immunohistochemistry.The reactive oxygen species (ros) level was detected by using a 2,7‐dichlorodihydrofluorescein diacetate ros assay kit.The in vivo effects of rb were evaluated in a xenograft mouse model.Rb treatment reduced cell viability and invasion in a dose‐dependent manner.Furthermore, rb also enhanced pyroptosis levels in a549 and h520 cells, as indicated by the increased release of ldh and pyroptosis‐related proteins.Interestingly, we also found that the antiproliferative and antimetastatic effects of rb were alleviated by the blockade of pyroptosis using nlrp3 inhibitor mcc950.Further study demonstrated that rb induced pyroptosis in a caspase‐1‐dependent manner, as evidenced by the finding that vx765 effectively reversed the effects of rb on a549 and h520 cells.We also found that rb could trigger caspase‐1‐dependent pyroptosis through ros‐mediated nf‐κb suppression.In summary, our findings provide a potential antitumor agent and a novel insight into the mechanism of rb treatment of nsclc.

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2020)
Publication types: Research Article;
Physcion 8-O-β-Glucopyranoside Exerts Anti-Tumor Activity Against Non-Small Cell Lung Cancer by Targeting PPARγ

Lung cancer is one of the most common causes of cancer related mortality.The present study is designed to investigate whether a naturally occurring anthraquinone compound, physcion 8‐o‐β‐glucopyranoside (pg) could exert anti‐cancer activity against non‐small cell lung cancer (nsclc).Cell viability was determined by cell counting kit‐8 (cck‐8) assay.Cell cycle distribution and cell apoptosis were determined by flow cytometry.Expressions of marker proteins were assessed by western blot analysis.To examine the role of pparγ (peroxisome proliferator‐activated receptor γ) in pg‐induced apoptosis and cell cycle arrest, pparγ was knockdown using si rna.In addition, a xenograft model was established to investigate the effect of pg in vivo.The results showed that pg markedly induced cell cycle arrest and apoptosis in human nsclc cell lines a549 and h358.The anti‐tumor effect of pg in nsclc cells was mediated by upregulation of pparγ.Besides, in nsclc cell lines, the anti‐cancer activity of pg was also examined in the xenograft mice model, which showed that pg could significantly reduce tumor burden and activate apoptotic signaling.Our results demonstrated that pg can be regarded as a candidate chemotherapeutic agent for lung cancer.Anat rec, 2018.© 2018 wiley periodicals, inc.Anat rec, 302:785–793, 2019.© 2018 wiley periodicals, inc.

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2018)
Publication types: Research Article;
Penfluridol triggers mitochondrial-mediated apoptosis and suppresses glycolysis in colorectal cancer cells through down-regulating hexokinase-2

Penfluridol, a commonly used antipsychotic agent in a clinical setting, exhibits potential anticancer properties against various human malignancies.Here, we investigated the effect of penfluridol on the biological behavior of colorectal cancer (crc) cells.Cell viability and clonogenic potential were detected by the cell counting kit‐8 and colony formation assay.The cell apoptosis and cell cycle distribution were quantified through flow cytometry.Caspase‐3 activity, glucose consumption, lactate production, and intracellular atp levels were evaluated using the corresponding commercial detection kits.The protein levels of related genes were detected through western blotting.Mitochondrial membrane potential was detected using jc‐1 staining.A crc xenograft tumor model was used to validate the antitumor activity of penfluridol in vivo.Penfluridol reduced cell survival and promoted apoptotic cell death effectively through the mitochondria‐mediated intrinsic pathway in a dose‐dependent manner.Furthermore, the process of glycolysis in hct‐116 and ht‐29 cells was inhibited upon penfluridol treatment, as evidenced by the decrease in glucose consumption, lactate production, and intracellular atp levels.Further mechanistic studies revealed that penfluridol influenced cell apoptosis and glycolysis in crc cells by downregulating hexokinase‐2 (hk‐2).The proapoptotic effect and glycolytic inhibition‐induced by penfluridol were effectively reversed by hk‐2 overexpression.Consistent with in vitro results, penfluridol could also suppress tumor growth and trigger apoptosis in vivo.Penfluridol triggers mitochondrial‐mediated apoptosis and induces glycolysis inhibition via modulating hk‐2 in crc and provides a theoretical basis to support penfluridol as a repurposed drug for crc patients.

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2020)
Publication types: Research Article;
Bufothionine Promotes Apoptosis via Triggering ER Stress and Synergizes with Temozolomide in Glioblastoma Multiforme Cells

Glioblastoma multiforme (gbm) is the most common type of malignant glioma.Bufothionine is one of the major active ingredients of cinobufacini.Although the antitumor activities of bufothionine have been reported, the underlying mechanism remains unclear.The present study showed that bufothionine exhibited antigrowth activities in gbm cell lines u87 and u373.Further investigation showed that bufothionine triggered endoplasmic reticulum (er) stress to promote apoptosis in u87 and u373 cells.Moreover, our results showed that bufothionine exhibited synergistic activities with temozolomide (tmz) to suppress the growth of u87 and u373 cells.The findings in the present study provide basis for further investigation of the therapeutic potential of bufothionine in gbm.Anat rec, 302:1950–1957, 2019.© 2019 american association for anatomy

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2019)
Publication types: Research Article;
PIM3 Functions as Oncogenic Factor and Promotes the Tumor Growth and Metastasis in Colorectal Cancer

Colorectal cancer (crc) is one of the common human malignancies.Discovery and identification of novel therapeutic target is imperative to improve the prognosis of crc patients.As a member of the pim family, pim3 has been found to be overexpressed in a variety of cancerous tumors.In this study, we evaluated the expression of pim3 in crc tissues and analyzed the role of pim3 in crc.Our results showed that pim3 expression was significantly higher in crc tissues compared with adjacent noncancerous tissues.The pim3 expression level was found to be correlated with advanced disease stage and lymph node metastasis.Moreover, pim3 was found to be able to predict poor prognosis in crc patients as an independent factor.In vitro studies also showed that knockdown of pim3 exhibited inhibitory effect on cell growth, promoted cell apoptosis and dampened invasive capability of hct116 and sw620 cells.Moreover, pim3 knockdown was able to delay tumor growth and suppress lung metastasis in xenograft model.Our results indicated that pim3 is a potential therapeutic target for crc.Anat rec, 302:1552–1560, 2019.© 2018 american association for anatomy

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2018)
Publication types: Research Article;
Huaier extract suppresses non-small cell lung cancer progression through activating NLRP3-dependent pyroptosis

Recent studies have reported the anticancer activity of huaier extract in various human malignancies.However, little is known about the effect of huaier extract in non‐small cell lung cancer (nsclc) and its underlying mechanism.The current study aimed to investigate whether huaier extract affects the progression of nsclc.M rna and proteins expression of pyroptotic‐related genes (nlrp3, caspase‐1, il‐1β, and il‐18) in nsclc tissues and cells were, respectively, detected by q rt‐pcr and western blot.The effects of huaier extract on nsclc cell viability and cytotoxicity were evaluated by cck‐8 assay, colony formation assay, and ldh detection kit.Besides, we established a xenograft model to assess the antitumor effect of huaier extract on tumor growth in vivo.Our results showed that the expression of pyroptotic‐related genes was downregulated in nsclc tissues and cell lines.Huaier extract pretreatment inhibited cell viability and the percentage of colony formation of h520 and h358 cells, and upregulated the expression of pyroptotic‐related genes.Mechanistically, huaier extract exhibited antitumor effect in nsclc via inducing nlrp3‐dependent pyroptosis in vitro and in vivo.In conclusion, our finding confirmed that huaier extract played an antitumor role in nsclc progression through promoting pyroptotic cell death, which provided a new potential strategy for nsclc clinical treatment.

Journal: The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology (2019)
Publication types: Research Article;