cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.19173970
title: RETRACTED ARTICLE: Somatostatin attenuates intestinal epithelial barrier injury during acute intestinal ischemia–reperfusion through Tollip/Myeloiddifferentiationfactor 88/Nuclear factor kappa-B signaling

description: We, the Editor and Publisher of <i>Bioengineered</i>, have retracted the following article: Tian, Y., Shu, R., Lei, Y., Xu, Y., Zhang, X., & Luo, H. (2022). Somatostatin attenuates intestinal epithelial barrier injury during acute intestinal ischemia–reperfusion through Tollip/Myeloiddifferentiationfactor 88/Nuclear factor kappa-B signaling. Bioengineered, 13(3), 5005–5020. https://doi.org/10.1080/21655979.2022.2038450 Following publication, the authors contacted the publisher to notify the journal that the study had failed its animal ethics approval review, and that there were additional concerns raised regarding the data. When contacted for further information, the authors were unable to address the concerns raised. In February 2025, concerns were raised by a third party regarding a mismatch between the study described and the ethics approval statement in the article. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our editorial policies and the COPE guidelines. The retracted articles will remain online to maintain the scholarly record, but they will be digitally watermarked on each page as ‘Retracted’.
DOI: 10.6084/m9.figshare.19164912
title: <i>Actinidia chinensis</i> Planch Root extract suppresses the growth and metastasis of hypopharyngeal carcinoma by inhibiting E2F Transcription Factor 1-mediated MNX1 antisense RNA 1

description: Increasing evidence has shown that traditional Chinese medicines and their bioactive components exert an anti-tumor effect, representing a novel treatment strategy. <i>Actinidia chinensis</i> Planch Root extracts (acRoots) have been reported to repress cancer cell proliferation and metastasis. The effect of acRoots on hypopharyngeal carcinoma progression was explored in this study. Firstly, data from MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and colony formation assays showed that incubation with accRoots reduced cell proliferation of hypopharyngeal carcinoma cells. Moreover, acRoots promoted the cell apoptosis of hypopharyngeal carcinoma. Secondly, cell migration and invasion of hypopharyngeal carcinoma cells were suppressed by acRoots. Thirdly, E2F1 (E2F Transcription Factor 1) and lncRNA MNX1-AS1 (MNX1 antisense RNA 1) were up-regulated in hypopharyngeal carcinoma tissues, and reduced in hypopharyngeal carcinoma cells post acRoots incubation. Overexpression of E2F1 attenuated acRoots-induced decrease in MNX1-AS1 in hypopharyngeal carcinoma cells. Lastly, administration with acRoots retarded in vivo hypopharyngeal carcinoma growth through down-regulation of E2F1-mediated MNX1-AS1. In conclusion, acRoots exerted tumor-suppressive role in hypopharyngeal carcinoma through inhibition of E2F1-mediated MNX1-AS1.
DOI: 10.6084/m9.figshare.19164912.v1
title: <i>Actinidia chinensis</i> Planch Root extract suppresses the growth and metastasis of hypopharyngeal carcinoma by inhibiting E2F Transcription Factor 1-mediated MNX1 antisense RNA 1

description: Increasing evidence has shown that traditional Chinese medicines and their bioactive components exert an anti-tumor effect, representing a novel treatment strategy. <i>Actinidia chinensis</i> Planch Root extracts (acRoots) have been reported to repress cancer cell proliferation and metastasis. The effect of acRoots on hypopharyngeal carcinoma progression was explored in this study. Firstly, data from MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and colony formation assays showed that incubation with accRoots reduced cell proliferation of hypopharyngeal carcinoma cells. Moreover, acRoots promoted the cell apoptosis of hypopharyngeal carcinoma. Secondly, cell migration and invasion of hypopharyngeal carcinoma cells were suppressed by acRoots. Thirdly, E2F1 (E2F Transcription Factor 1) and lncRNA MNX1-AS1 (MNX1 antisense RNA 1) were up-regulated in hypopharyngeal carcinoma tissues, and reduced in hypopharyngeal carcinoma cells post acRoots incubation. Overexpression of E2F1 attenuated acRoots-induced decrease in MNX1-AS1 in hypopharyngeal carcinoma cells. Lastly, administration with acRoots retarded in vivo hypopharyngeal carcinoma growth through down-regulation of E2F1-mediated MNX1-AS1. In conclusion, acRoots exerted tumor-suppressive role in hypopharyngeal carcinoma through inhibition of E2F1-mediated MNX1-AS1.
DOI: 10.6084/m9.figshare.19173970.v1
title: Somatostatin attenuates intestinal epithelial barrier injury during acute intestinal ischemia–reperfusion through Tollip/Myeloiddifferentiationfactor 88/Nuclear factor kappa-B signaling

description: In the process of ischemia–reperfusion injury, intestinal ischemia and inflammation interweave, leading to tissue damage or necrosis. However, oxygen radicals and inflammatory mediators produced after reperfusion cause tissue damage again, resulting in severe intestinal epithelial barrier dysfunction. The aim of this study was to determine the protective effect of somatostatin on intestinal epithelial barrier function during intestinal ischemia–reperfusion injury and explore its mechanism. By establishing a rat intestinal ischemia–reperfusion model, pretreating the rats with somatostatin, and then detecting the histopathological changes, intestinal permeability and expression of tight junction proteins in intestinal tissues, the protective effect of somatostatin on the intestinal epithelial barrier was measured in vivo. The mechanism was determined in interferon γ (IFN-γ)-treated Caco-2 cells in vitro. The results showed that somatostatin could ameliorate ischemia–reperfusion-induced intestinal epithelial barrier dysfunction and protect Caco-2 cells against IFN-γ-induced decreases in tight junction protein expression and increases in monolayer cell permeability. The expression of Tollip was upregulated by somatostatin both in ischemia–reperfusion rats and IFN-γ-treated Caco-2 cells, while the activation of TLR2/MyD88/NF-κB signaling was inhibited by somatostatin. Tollip inhibition reversed the protective effect of somatostatin on the intestinal epithelial barrier. In conclusion, somatostatin could attenuate ischemia–reperfusion-induced intestinal epithelial barrier injury by inhibiting the activation of TLR2/MyD88/NF-κB signaling through upregulation of Tollip.
DOI: 10.6084/m9.figshare.19173970.v2
title: RETRACTED ARTICLE: Somatostatin attenuates intestinal epithelial barrier injury during acute intestinal ischemia–reperfusion through Tollip/Myeloiddifferentiationfactor 88/Nuclear factor kappa-B signaling

description: We, the Editor and Publisher of <i>Bioengineered</i>, have retracted the following article: Tian, Y., Shu, R., Lei, Y., Xu, Y., Zhang, X., & Luo, H. (2022). Somatostatin attenuates intestinal epithelial barrier injury during acute intestinal ischemia–reperfusion through Tollip/Myeloiddifferentiationfactor 88/Nuclear factor kappa-B signaling. Bioengineered, 13(3), 5005–5020. https://doi.org/10.1080/21655979.2022.2038450 Following publication, the authors contacted the publisher to notify the journal that the study had failed its animal ethics approval review, and that there were additional concerns raised regarding the data. When contacted for further information, the authors were unable to address the concerns raised. In February 2025, concerns were raised by a third party regarding a mismatch between the study described and the ethics approval statement in the article. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our editorial policies and the COPE guidelines. The retracted articles will remain online to maintain the scholarly record, but they will be digitally watermarked on each page as ‘Retracted’.
DOI: 10.6084/m9.figshare.19237153
title: Circular RNA midline-1 (circMID1) promotes proliferation, migration, invasion and glycolysis in prostate cancer

description: The key role of circular RNA (circRNA) in the malignant progression of cancers has been demonstrated. However, the role of circRNA midline-1 (circMID1) in prostate cancer (PCa) progression has not been clarified. Quantitative real-time PCR was used to measure relative expression. Function analysis was performed using EdU staining, colony formation assay, flow cytometry, wound healing assay, transwell assay and cell glycolysis detection. The protein levels were detected by Western blot analysis. RNA pull-down assay, dual-luciferase reporter assay and RIP assay were performed to verify RNA interaction. Animal experiments were utilized to explore the effects of circMID1 knockdown on PCa tumorigenesis in vivo. Our results showed that circMID1 was upregulated in PCa tissues and cells and its knockdown inhibited PCa cell proliferation, migration, invasion and glycolysis in vitro, as well as PCa tumorigenesis in vivo. IGF1R and YTHDC2 were highly expressed in PCa tissues and cells, and their expression was positively regulated by circMID1. IGF1R and YTHDC2 overexpression reversed the inhibitory effect of circMID1 silencing on PCa cell progression. In terms of mechanism, circMID1 could sponge miR-330-3p and miR-330-3p could target IGF1R and YTHDC2. Functional experiments showed that circMID1 sponged miR-330-3p to regulate PCa progression via the YTHDC2/IGF1R/AKT axis. In conclusion, our data confirmed that circMID1 might play a pro-cancer role in PCa, which promoted PCa progression through regulating the miR-330-3p/YTHDC2/IGF1R/AKT axis.
DOI: 10.6084/m9.figshare.19237153.v1
title: Circular RNA midline-1 (circMID1) promotes proliferation, migration, invasion and glycolysis in prostate cancer

description: The key role of circular RNA (circRNA) in the malignant progression of cancers has been demonstrated. However, the role of circRNA midline-1 (circMID1) in prostate cancer (PCa) progression has not been clarified. Quantitative real-time PCR was used to measure relative expression. Function analysis was performed using EdU staining, colony formation assay, flow cytometry, wound healing assay, transwell assay and cell glycolysis detection. The protein levels were detected by Western blot analysis. RNA pull-down assay, dual-luciferase reporter assay and RIP assay were performed to verify RNA interaction. Animal experiments were utilized to explore the effects of circMID1 knockdown on PCa tumorigenesis in vivo. Our results showed that circMID1 was upregulated in PCa tissues and cells and its knockdown inhibited PCa cell proliferation, migration, invasion and glycolysis in vitro, as well as PCa tumorigenesis in vivo. IGF1R and YTHDC2 were highly expressed in PCa tissues and cells, and their expression was positively regulated by circMID1. IGF1R and YTHDC2 overexpression reversed the inhibitory effect of circMID1 silencing on PCa cell progression. In terms of mechanism, circMID1 could sponge miR-330-3p and miR-330-3p could target IGF1R and YTHDC2. Functional experiments showed that circMID1 sponged miR-330-3p to regulate PCa progression via the YTHDC2/IGF1R/AKT axis. In conclusion, our data confirmed that circMID1 might play a pro-cancer role in PCa, which promoted PCa progression through regulating the miR-330-3p/YTHDC2/IGF1R/AKT axis.
DOI: 10.6084/m9.figshare.19336828
title: Long non-coding RNA long intergenic non-coding 00641 mediates cell progression with stimulating cisplatin-resistance in osteosarcoma cells via microRNA-320d/myeloid cell leukemia-1 axis

description: As a staple chemotherapy medicine, cisplatin (DDP) is extensively applied in cancer patients, but its drug resistance is limited. Numerous studies have elucidated that long non-coding RNA (lncRNA) performs as a pivotal agent in osteosarcoma (OS). Nevertheless, lncRNA long intergenic non-coding 00641 (LINC00641)’s functions in DDP resistance for OS remain obscure. The purpose of this study was to investigate the effect and mechanism of LINC00641 on drug resistance of OS. The tissues of both clinical cancer patients and the normal control were gathered. Detection of LINC00641, microRNA-320d (miR-320d) and myeloid cell leukemia-1 (MCL1) was conducted. After the selection of OS cell lines, the detection of cell advancement was applied. Series of experiments were conducted to verify the interaction of LINC00641, miR-320d and MCL1. Xenografted tumor model <i>in vivo</i> was utilized to determine the function of LINC00641. The data displayed, LINC00641 was prominently elevated in OS tissues and cells, especially in DDP-resistant tumors and cell lines. Knock-down LINC00641 was able to attenuate progression of DDP-resistant OS cells thus dampening their drug resistance toward DDP. Moreover, knock-downing LINC00641 gene was also able to manifest antagonism toward DDP-resistance <i>in vivo</i>. On the grounds of bioinformatics prediction, a direct binding of LINC00641 with miR-320d existed, whose target was MCL1. Meanwhile, LINC00641 modulated MCL1 via targeting miR-320d. Additionally, repressive LINC00641 blocked MCL1 via emulative interaction with miR-320d, thus expediting DDP-sensitivity of OS cells. All in all, it is found that LINC00641 is available to escalate drug resistance of DDP-resistant OS cells via mediation of miR-320d/MCL1 axis.
DOI: 10.6084/m9.figshare.19336828.v1
title: Long non-coding RNA long intergenic non-coding 00641 mediates cell progression with stimulating cisplatin-resistance in osteosarcoma cells via microRNA-320d/myeloid cell leukemia-1 axis

description: As a staple chemotherapy medicine, cisplatin (DDP) is extensively applied in cancer patients, but its drug resistance is limited. Numerous studies have elucidated that long non-coding RNA (lncRNA) performs as a pivotal agent in osteosarcoma (OS). Nevertheless, lncRNA long intergenic non-coding 00641 (LINC00641)’s functions in DDP resistance for OS remain obscure. The purpose of this study was to investigate the effect and mechanism of LINC00641 on drug resistance of OS. The tissues of both clinical cancer patients and the normal control were gathered. Detection of LINC00641, microRNA-320d (miR-320d) and myeloid cell leukemia-1 (MCL1) was conducted. After the selection of OS cell lines, the detection of cell advancement was applied. Series of experiments were conducted to verify the interaction of LINC00641, miR-320d and MCL1. Xenografted tumor model <i>in vivo</i> was utilized to determine the function of LINC00641. The data displayed, LINC00641 was prominently elevated in OS tissues and cells, especially in DDP-resistant tumors and cell lines. Knock-down LINC00641 was able to attenuate progression of DDP-resistant OS cells thus dampening their drug resistance toward DDP. Moreover, knock-downing LINC00641 gene was also able to manifest antagonism toward DDP-resistance <i>in vivo</i>. On the grounds of bioinformatics prediction, a direct binding of LINC00641 with miR-320d existed, whose target was MCL1. Meanwhile, LINC00641 modulated MCL1 via targeting miR-320d. Additionally, repressive LINC00641 blocked MCL1 via emulative interaction with miR-320d, thus expediting DDP-sensitivity of OS cells. All in all, it is found that LINC00641 is available to escalate drug resistance of DDP-resistant OS cells via mediation of miR-320d/MCL1 axis.
DOI: 10.6084/m9.figshare.19203477
title: Enhancer of zeste homolog 2 promotes hepatocellular cancer progression and chemoresistance by enhancing protein kinase B activation through microRNA-381-mediated SET domain bifurcated 1

description: Metastasis and chemoresistance are the leading causes of death in patients with hepatocellular carcinoma (HCC). microRNAs (miRNAs or miRs) may be useful as diagnostic, therapeutic and prognostic markers for HCC. In this study, we set out to investigate the possible role of miR-381 in HCC development and chemoresistance along with the related mechanism. Microarray-based gene expression profiling was carried out to analyze the expression of SET domain bifurcated 1 (SETDB1) and histone methyltransferase enhancer of zeste homolog 2 (EZH2) followed by validation in clinical HCC tissues and cells. The potential binding between miR-381 and SETDB1 was found and verified. Then, the role of SETDB1 in HCC in relation to miR-381 and protein kinase B (AKT) pathway was explored through gain- and loss-of-function approaches. After expression determination of EZH2, SETDB1, miR-381, and AKT pathway-related factors, their reactions were analyzed and their functional roles in HCC progression and chemoresistance were investigated <i>in vitro</i> and <i>in vivo</i>. SETDB1 was aberrantly upregulated in clinical HCC tissues and cells. This upregulation activated AKT pathway by promoting its tri-methylation on K64. SETDB1 promoted the proliferation, migration and chemoresistance through the AKT pathway in HCC cells. In a xenograft mouse model, SETDB1 promoted HCC cell tumorigenesis <i>in vivo</i> by activating the AKT pathway. Furthermore, EZH2 suppressed miR-381 by catalyzing the activity of H3K27me3 on its promoter region. In conclusion, EZH2 suppressed miR-381 expression by promoting H3K27me3 activity on its promoter region to facilitate SETDB1 expression, thereby activating the AKT pathway to promote hepatocarcinogenesis and chemoresistance.
DOI: 10.6084/m9.figshare.19203477.v1
title: Enhancer of zeste homolog 2 promotes hepatocellular cancer progression and chemoresistance by enhancing protein kinase B activation through microRNA-381-mediated SET domain bifurcated 1

description: Metastasis and chemoresistance are the leading causes of death in patients with hepatocellular carcinoma (HCC). microRNAs (miRNAs or miRs) may be useful as diagnostic, therapeutic and prognostic markers for HCC. In this study, we set out to investigate the possible role of miR-381 in HCC development and chemoresistance along with the related mechanism. Microarray-based gene expression profiling was carried out to analyze the expression of SET domain bifurcated 1 (SETDB1) and histone methyltransferase enhancer of zeste homolog 2 (EZH2) followed by validation in clinical HCC tissues and cells. The potential binding between miR-381 and SETDB1 was found and verified. Then, the role of SETDB1 in HCC in relation to miR-381 and protein kinase B (AKT) pathway was explored through gain- and loss-of-function approaches. After expression determination of EZH2, SETDB1, miR-381, and AKT pathway-related factors, their reactions were analyzed and their functional roles in HCC progression and chemoresistance were investigated <i>in vitro</i> and <i>in vivo</i>. SETDB1 was aberrantly upregulated in clinical HCC tissues and cells. This upregulation activated AKT pathway by promoting its tri-methylation on K64. SETDB1 promoted the proliferation, migration and chemoresistance through the AKT pathway in HCC cells. In a xenograft mouse model, SETDB1 promoted HCC cell tumorigenesis <i>in vivo</i> by activating the AKT pathway. Furthermore, EZH2 suppressed miR-381 by catalyzing the activity of H3K27me3 on its promoter region. In conclusion, EZH2 suppressed miR-381 expression by promoting H3K27me3 activity on its promoter region to facilitate SETDB1 expression, thereby activating the AKT pathway to promote hepatocarcinogenesis and chemoresistance.
DOI: 10.6084/m9.figshare.19336504
title: Knockdown of circ_0001679 alleviates lipopolysaccharide-induced MLE-12 lung cell injury by regulating the miR-338-3p/ mitogen-activated protein kinase 1 axis

description: The upregulation of circ_0001679 was reported in lipopolysaccharide (LPS)-induced lung injury mouse model, but its functional roles and mechanisms in LPS-induced lung injury remain to be investigated. In this study, we aimed to explore the potential role of circ_0001679 in septic acute lung injury. We initially established an <i>in vitro</i> lung cell injury model using LPS-treated MLE-12 cells. siRNAs targeting circRNA_0001679 were employed to stably knock down circRNA_0001679, followed by functional assays to investigate the effect of circRNA_0001679 silencing. The levels of inflammatory cytokines such as IL-6, IL-β and TNF-α (Tumor necrosis factor-α) were detected by ELISA (Enzyme-linked immunosorbent assay). Meanwhile, protein levels of Bcl-2, cleaved-caspase 3, Bax, and MAPK1 (Mitogen-Activated Protein Kinase 1) proteins expression level were measured by Western blot. We found that Circ_0001679 was upregulated in LPS-induced MLE-12 cells, and silencing circ_0001679 attenuated the growth inhibition and suppressed apoptosis induced by LPS. Circ_0001679 knockdown also lowered levels of IL-6, IL-β and TNF-α, and prevent the activation of cleaved-caspase 3 protein. We further revealed that circ_0001679 functioned as a sponge of miR-338-3p to negatively regulate miR-338-3p activity. miR-338-3p downregulated its downstream target MAPK1, while the upregulation of circ_0001679 maintained a high-level expression of MAPK1 by suppressing miR-338-3p. Collectively, our study indicates that circ_0001679/miR-338-3p/MAPK1 axis may play an important role in the pathogenesis of acute lung injury (ALI).
DOI: 10.6084/m9.figshare.19336504.v1
title: Knockdown of circ_0001679 alleviates lipopolysaccharide-induced MLE-12 lung cell injury by regulating the miR-338-3p/ mitogen-activated protein kinase 1 axis

description: The upregulation of circ_0001679 was reported in lipopolysaccharide (LPS)-induced lung injury mouse model, but its functional roles and mechanisms in LPS-induced lung injury remain to be investigated. In this study, we aimed to explore the potential role of circ_0001679 in septic acute lung injury. We initially established an <i>in vitro</i> lung cell injury model using LPS-treated MLE-12 cells. siRNAs targeting circRNA_0001679 were employed to stably knock down circRNA_0001679, followed by functional assays to investigate the effect of circRNA_0001679 silencing. The levels of inflammatory cytokines such as IL-6, IL-β and TNF-α (Tumor necrosis factor-α) were detected by ELISA (Enzyme-linked immunosorbent assay). Meanwhile, protein levels of Bcl-2, cleaved-caspase 3, Bax, and MAPK1 (Mitogen-Activated Protein Kinase 1) proteins expression level were measured by Western blot. We found that Circ_0001679 was upregulated in LPS-induced MLE-12 cells, and silencing circ_0001679 attenuated the growth inhibition and suppressed apoptosis induced by LPS. Circ_0001679 knockdown also lowered levels of IL-6, IL-β and TNF-α, and prevent the activation of cleaved-caspase 3 protein. We further revealed that circ_0001679 functioned as a sponge of miR-338-3p to negatively regulate miR-338-3p activity. miR-338-3p downregulated its downstream target MAPK1, while the upregulation of circ_0001679 maintained a high-level expression of MAPK1 by suppressing miR-338-3p. Collectively, our study indicates that circ_0001679/miR-338-3p/MAPK1 axis may play an important role in the pathogenesis of acute lung injury (ALI).