Image_1_Research on the effects of rs1800566 C/T polymorphism of NAD(P)H quinone oxidoreductase 1 gene on cancer risk involves analysis of 43,736 cancer cases and 56,173 controls.tif

ObjectiveA two-electron reductase known as NQO1 [NAD(P)H quinone oxidoreductase 1] is regarded as an excellent anticancer target. Studies have found that rs1800566 polymorphism of NQO1 is linked to different cancers, but their associations remain controversial.MethodsIn the present work, we selected to do a comprehensive meta-analysis to analyze their correlation. We performed searches on PubMed, Embase, Google Scholar, Chinese database, and Web of Science. The results we obtained covered all publications before April 3, 2022.ResultsThere were 176 case-control studies among them, with 56,173 corresponding controls and 43,736 cancer cases. We determined that the NQO1 rs1800566 polymorphism was not related to the cancer risk by calculating 95% confidence intervals and odds ratios. However, stratified genotyping showed that this polymorphism was protective against hepatocellular carcinoma, renal cell carcinoma, and gastric cancer. In addition, on dividing cancer into six systems, the association with gastrointestinal cancer decreased. In the race-based subgroup, a decreasing trend was observed in Asians, while an increasing trend was found among Caucasians, Africans, and mixed populations. The decreased correlation in the hospital-based subgroup was also detected.ConclusionCurrent study shows that rs1800566 polymorphism of NQO1 was linked to cancer susceptibility and maybe as a tumor marker in their development.</p

Table_1_Research on the effects of rs1800566 C/T polymorphism of NAD(P)H quinone oxidoreductase 1 gene on cancer risk involves analysis of 43,736 cancer cases and 56,173 controls.docx

ObjectiveA two-electron reductase known as NQO1 [NAD(P)H quinone oxidoreductase 1] is regarded as an excellent anticancer target. Studies have found that rs1800566 polymorphism of NQO1 is linked to different cancers, but their associations remain controversial.MethodsIn the present work, we selected to do a comprehensive meta-analysis to analyze their correlation. We performed searches on PubMed, Embase, Google Scholar, Chinese database, and Web of Science. The results we obtained covered all publications before April 3, 2022.ResultsThere were 176 case-control studies among them, with 56,173 corresponding controls and 43,736 cancer cases. We determined that the NQO1 rs1800566 polymorphism was not related to the cancer risk by calculating 95% confidence intervals and odds ratios. However, stratified genotyping showed that this polymorphism was protective against hepatocellular carcinoma, renal cell carcinoma, and gastric cancer. In addition, on dividing cancer into six systems, the association with gastrointestinal cancer decreased. In the race-based subgroup, a decreasing trend was observed in Asians, while an increasing trend was found among Caucasians, Africans, and mixed populations. The decreased correlation in the hospital-based subgroup was also detected.ConclusionCurrent study shows that rs1800566 polymorphism of NQO1 was linked to cancer susceptibility and maybe as a tumor marker in their development.</p

DataSheet_3_Upregulation of COPB2 Promotes Prostate Cancer Proliferation and Invasion Through the MAPK/TGF-β Signaling Pathway.xlsx

There is increasing evidence that coatomer protein complex subunit beta 2 (COPB2) plays an important role in various cancer types. This study explored the role and the downstream mediators of COPB2 in prostate cancer (PCa). The expression of COPB2 was determined by the Cancer Genome Atlas database and enzyme-linked immunosorbent assay. COPB2 expression was upregulated in PCa tissues and correlated with Gleason score, biochemical recurrence, and poor prognosis. The functional roles of COPB2 in PCa were verified through a series of experiments. Knocking down COPB2 expression inhibited the growth and clonogenesis of PCa cells, promoted cell apoptosis, and inhibited the ability of scratch repair, invasion of PCa cells, and tumor growth in Nude mice. To analyze downstream signaling pathways, ingenuity pathway analysis, GSEA, and whole-genome expression spectrum GeneChip analysis were used. Western blot revealed that COPB2 expression promoted the proliferation and invasion of PCa cells by regulating the MAPK/TGF-β signaling pathway. The interacting protein (nuclear protein 1, NUPR1) was identified via Co-IP, real-time PCR, Western blot, and TCGA database in sampled tissues. The expressions of the interaction proteins NUPR1 and COPB2 were negatively regulated by each other. COPB2 could be a new biomarker for PCa diagnosis and monitoring and to provide a theoretical basis for identifying effective drug intervention targets through in-depth mechanistic studies.</p

DataSheet_4_Upregulation of COPB2 Promotes Prostate Cancer Proliferation and Invasion Through the MAPK/TGF-β Signaling Pathway.pdf

There is increasing evidence that coatomer protein complex subunit beta 2 (COPB2) plays an important role in various cancer types. This study explored the role and the downstream mediators of COPB2 in prostate cancer (PCa). The expression of COPB2 was determined by the Cancer Genome Atlas database and enzyme-linked immunosorbent assay. COPB2 expression was upregulated in PCa tissues and correlated with Gleason score, biochemical recurrence, and poor prognosis. The functional roles of COPB2 in PCa were verified through a series of experiments. Knocking down COPB2 expression inhibited the growth and clonogenesis of PCa cells, promoted cell apoptosis, and inhibited the ability of scratch repair, invasion of PCa cells, and tumor growth in Nude mice. To analyze downstream signaling pathways, ingenuity pathway analysis, GSEA, and whole-genome expression spectrum GeneChip analysis were used. Western blot revealed that COPB2 expression promoted the proliferation and invasion of PCa cells by regulating the MAPK/TGF-β signaling pathway. The interacting protein (nuclear protein 1, NUPR1) was identified via Co-IP, real-time PCR, Western blot, and TCGA database in sampled tissues. The expressions of the interaction proteins NUPR1 and COPB2 were negatively regulated by each other. COPB2 could be a new biomarker for PCa diagnosis and monitoring and to provide a theoretical basis for identifying effective drug intervention targets through in-depth mechanistic studies.</p

DataSheet_1_Upregulation of COPB2 Promotes Prostate Cancer Proliferation and Invasion Through the MAPK/TGF-β Signaling Pathway.docx

There is increasing evidence that coatomer protein complex subunit beta 2 (COPB2) plays an important role in various cancer types. This study explored the role and the downstream mediators of COPB2 in prostate cancer (PCa). The expression of COPB2 was determined by the Cancer Genome Atlas database and enzyme-linked immunosorbent assay. COPB2 expression was upregulated in PCa tissues and correlated with Gleason score, biochemical recurrence, and poor prognosis. The functional roles of COPB2 in PCa were verified through a series of experiments. Knocking down COPB2 expression inhibited the growth and clonogenesis of PCa cells, promoted cell apoptosis, and inhibited the ability of scratch repair, invasion of PCa cells, and tumor growth in Nude mice. To analyze downstream signaling pathways, ingenuity pathway analysis, GSEA, and whole-genome expression spectrum GeneChip analysis were used. Western blot revealed that COPB2 expression promoted the proliferation and invasion of PCa cells by regulating the MAPK/TGF-β signaling pathway. The interacting protein (nuclear protein 1, NUPR1) was identified via Co-IP, real-time PCR, Western blot, and TCGA database in sampled tissues. The expressions of the interaction proteins NUPR1 and COPB2 were negatively regulated by each other. COPB2 could be a new biomarker for PCa diagnosis and monitoring and to provide a theoretical basis for identifying effective drug intervention targets through in-depth mechanistic studies.</p

DataSheet_2_Upregulation of COPB2 Promotes Prostate Cancer Proliferation and Invasion Through the MAPK/TGF-β Signaling Pathway.pdf

There is increasing evidence that coatomer protein complex subunit beta 2 (COPB2) plays an important role in various cancer types. This study explored the role and the downstream mediators of COPB2 in prostate cancer (PCa). The expression of COPB2 was determined by the Cancer Genome Atlas database and enzyme-linked immunosorbent assay. COPB2 expression was upregulated in PCa tissues and correlated with Gleason score, biochemical recurrence, and poor prognosis. The functional roles of COPB2 in PCa were verified through a series of experiments. Knocking down COPB2 expression inhibited the growth and clonogenesis of PCa cells, promoted cell apoptosis, and inhibited the ability of scratch repair, invasion of PCa cells, and tumor growth in Nude mice. To analyze downstream signaling pathways, ingenuity pathway analysis, GSEA, and whole-genome expression spectrum GeneChip analysis were used. Western blot revealed that COPB2 expression promoted the proliferation and invasion of PCa cells by regulating the MAPK/TGF-β signaling pathway. The interacting protein (nuclear protein 1, NUPR1) was identified via Co-IP, real-time PCR, Western blot, and TCGA database in sampled tissues. The expressions of the interaction proteins NUPR1 and COPB2 were negatively regulated by each other. COPB2 could be a new biomarker for PCa diagnosis and monitoring and to provide a theoretical basis for identifying effective drug intervention targets through in-depth mechanistic studies.</p

Large-Area Ultrastrong and Stiff Layered MXene Nanocomposites by Shear-Flow-Induced Alignment of Nanosheets

To shield increasingly severe radiation pollution, ultrathin MXene-based electromagnetic interference (EMI) shielding materials with excellent mechanical properties are urgently demanded in wearable electrical devices or aerospace fields. However, it is still a challenge to fabricate ultrastrong and stiff MXene-based nanocomposites with excellent EMI shielding capacity in a universal and scalable manner. Here, inspired by the natural nacre structure, we propose an efficient superspreading strategy to construct a highly oriented layered “brick-and-mortar” structure using shear-flow-induced alignment of MXene nanosheets at an immiscible hydrogel/oil interface. A continuous and large-area MXene nanocomposite film has been fabricated through a homemade industrial-scale continuous fabrication setup. The prepared MXene nanocomposite films exhibit a tensile strength of 647.6 ± 56 MPa and a Young’s modulus of 59.8 ± 6.1 GPa, respectively. These outstanding mechanical properties are attributed to the continuous interphase layer that formed between the well-aligned MXene nanosheets. Moreover, the obtained MXene nanocomposites also show great EMI shielding effectiveness (51.6 dB). We consider that our MXene-based nanocomposite films may be potentially applied as electrical or aerospace devices with superior mechanical properties and high EMI shielding capacity

Large-Area Ultrastrong and Stiff Layered MXene Nanocomposites by Shear-Flow-Induced Alignment of Nanosheets

To shield increasingly severe radiation pollution, ultrathin MXene-based electromagnetic interference (EMI) shielding materials with excellent mechanical properties are urgently demanded in wearable electrical devices or aerospace fields. However, it is still a challenge to fabricate ultrastrong and stiff MXene-based nanocomposites with excellent EMI shielding capacity in a universal and scalable manner. Here, inspired by the natural nacre structure, we propose an efficient superspreading strategy to construct a highly oriented layered “brick-and-mortar” structure using shear-flow-induced alignment of MXene nanosheets at an immiscible hydrogel/oil interface. A continuous and large-area MXene nanocomposite film has been fabricated through a homemade industrial-scale continuous fabrication setup. The prepared MXene nanocomposite films exhibit a tensile strength of 647.6 ± 56 MPa and a Young’s modulus of 59.8 ± 6.1 GPa, respectively. These outstanding mechanical properties are attributed to the continuous interphase layer that formed between the well-aligned MXene nanosheets. Moreover, the obtained MXene nanocomposites also show great EMI shielding effectiveness (51.6 dB). We consider that our MXene-based nanocomposite films may be potentially applied as electrical or aerospace devices with superior mechanical properties and high EMI shielding capacity