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Correction: m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting miR-107/LATS2–mediated YAP activity in NSCLC
Molecular Cancer ( IF 27.7 ) Pub Date : 2022-06-13 , DOI: 10.1186/s12943-022-01593-x
Dan Jin 1 , Jiwei Guo 2 , Yan Wu 2 , Lijuan Yang 2 , Xiaohong Wang 3 , Jing Du 2 , Juanjuan Dai 2 , Weiwei Chen 2 , Kaikai Gong 2 , Shuang Miao 2 , Xuelin Li 2 , Hongliang Sun 4
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Correction: Mol Cancer 19, 40 (2020)

https://doi.org/10.1186/s12943-020-01161-1

Following publication of the original article [1], the authors identified minor errors in Figs. 1 and 5; specifically:

Fig. 1
figure 1

Ectopic expression of YAP and ALKBH5 regulates cell proliferation, invasion, migration, and EMT in NSCLC cells. a The mRNA and protein levels of YAP and ALKBH5 were analyzed by RT-PCR and western blot assays in the paired fresh NSCLC tumor cancer tissues (Tumor) and matched adjacent normal tissues (Normal) (left panel, n = 10; right panel, n = 30). b The expressions of YAP and ALKBH5 were analyzed by immunohistochemical (IHC) assay in the human lung cancer tissues and their normal adjacent lung tissues (n = 5). c The TCGA database indicated that YAP was higher but ALKBH5 was lower in tumor tissues than their normal tissues. d The mRNA and protein levels of YAP and ALKBH5 were analyzed by RT-PCR, qPCR and western blot assays in NSCLC cell lines and their control (normal) cell, BEAS-2B. e High expression of YAP (P = 0.00932) but low expression of ALKBH5 (P = 0.00545) were associated with worse prognosis for NSCLC patients. (f-j) A549 cells were transfected with indicated genes of YAP and ALKBH5. f The expressions of YAP and ALKBH5 were analyzed by RT-PCR and western blot assays. g The cellular growth was analyzed by CCK8 assay. h The migration viability was analyzed by scratch assay. (i) The cellular invasion and migration growths were analyzed by transwell assay. j The expressions of E-cadherin and Vimentin were analyzed by RT-PCR and western blot assays. Results were presented as mean ± SD of three independent experiments. *P < 0.05 or **P < 0.01 indicates a significant difference between the indicated groups

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Fig. 5
figure 2

YTHDF1-promoted YAP mRNA translation is regulated by m6A modification and interaction with eIF3a. a The mRNA and protein levels of YTHDF1 were analyzed by RT-PCR and western blot assays in paired fresh NSCLC tumor cancer tissues (Tumor) and matched adjacent normal tissues (Normal) (left panel, n = 10; right panel, n = 30). b The expression of YTHDF1 was analyzed by IHC assay in the different grades of lung cancer tissues. c High expression of YTHDF1 is associated with worse prognosis for NSCLC patients (P = 0.018). (d, e) A549 cells were transfected with indicated genes of YTHDF1. d The migration growth was analyzed by scratch assay. e The expressions of E-cadherin and Vimentin were analyzed by western blot assay. f The xenografted tumors (left panel) and the metastasizing lung tumors (right panel) originated from A549 cells with stable expression of indicated genes constructed by subcutaneous injection. g The protein levels of YAP, CTGF and Cyr61 were analyzed in A549 cells determined by WB assay. h Co-IPs performed using lysates collected from A549 cells with immunoprecipitation by either YTHDF1 or eIF3a antibodies. (i-k) The protein level of YAP was analyzed by ELISA assay in puromycin treated A549 cells with transfection with indicated genes. (l-p) A549 cell were transfected with indicated genes of YTHDF1 and YAP. l The protein levels of YTHDF1, YAP, CTGF and Cyr61 were analyzed by western blot assay. m The size and number of colons were analyzed by colony formation assay. n The cellular invasion and migration growth were analyzed by transwell assay. o The expressions of E-cadherin and Vimentin were analyzed by qPCR assay. p The relative of cleaved Caspas-3 was analyzed by western blot assay. Results were presented as mean ± SD of three independent experiments. *P < 0.05 or **P < 0.01 indicates a significant difference between the indicated groups. ns, not significant

Full size image

Fig. 1b: Incorrect image used to show expression of ALKBH5 Tumor group (bottom right panel); the correct image is now used.

Fig. 5 h: Incorrect image was used for the YTHDF1 band; the correct band is now used.

The corrected figures are given here. The correction does not have any effect on the final conclusions of the paper. The original article has been corrected.

  1. Jin D, Guo J, Wu Y, et al. m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting miR-107/LATS2–mediated YAP activity in NSCLC. Mol Cancer. 2020;19:40. https://doi.org/10.1186/s12943-020-01161-1.

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Author notes
  1. Dan Jin and Jiwei Guo contributed equally to this work.

Authors and Affiliations

  1. Clinical Medical Laboratory, Binzhou Medical University Hospital, Binzhou, 256603, People’s Republic of China

    Dan Jin

  2. Cancer research institute, Binzhou Medical University Hospital, Binzhou, 256603, People’s Republic of China

    Jiwei Guo, Yan Wu, Lijuan Yang, Jing Du, Juanjuan Dai, Weiwei Chen, Kaikai Gong, Shuang Miao & Xuelin Li

  3. Department of Thyroid and Breast Surgery, Binzhou Medical University Hospital, Binzhou, 256603, People’s Republic of China

    Xiaohong Wang

  4. Department of reproductive medicine, Binzhou Medical University Hospital, Binzhou, 256603, People’s Republic of China

    Hongliang Sun

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Correspondence to Jiwei Guo.

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Jin, D., Guo, J., Wu, Y. et al. Correction: m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting miR-107/LATS2–mediated YAP activity in NSCLC. Mol Cancer 21, 130 (2022). https://doi.org/10.1186/s12943-022-01593-x

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中文翻译:

更正:m6A 去甲基化酶 ALKBH5 通过降低 YTHDFs 介导的 YAP 表达和抑制 NSCLC 中 miR-107/LATS2 介导的 YAP 活性来抑制肿瘤生长和转移

更正:Mol Cancer 19, 40 (2020)

https://doi.org/10.1186/s12943-020-01161-1

在发表原始文章 [1] 后,作者发现了图 1 和 2 中的小错误。1和5;具体来说:

图。1
图1

YAP 和 ALKBH5 的异位表达调节 NSCLC 细胞中的细胞增殖、侵袭、迁移和 EMT。a在配对的新鲜 NSCLC 肿瘤组织 (Tumor) 和匹配的相邻正常组织 (Normal) 中,通过 RT-PCR 和蛋白质印迹分析分析 YAP 和 ALKBH5 的 mRNA 和蛋白质水平(左图,n = 10;右图,n = 30)。b通过免疫组化(IHC)法分析人肺癌组织及其正常肺组织( n = 5)中YAP和ALKBH5的表达。c TCGA 数据库表明肿瘤组织中的 YAP 高于正常组织,但 ALKBH5 低于正常组织。d在 NSCLC 细胞系及其对照(正常)细胞 BEAS-2B 中,通过 RT-PCR、qPCR 和蛋白质印迹分析分析 YAP 和 ALKBH5 的 mRNA 和蛋白质水平。e YAP 高表达 ( P = 0.00932) 但 ALKBH5 低表达 ( P = 0.00545) 与 NSCLC 患者预后较差有关。(fj) 用指定的 YAP 和 ALKBH5 基因转染 A549 细胞。f通过 RT-PCR 和蛋白质印迹分析分析 YAP 和 ALKBH5 的表达。g通过CCK8测定分析细胞生长。h通过划痕法分析迁移活力。(i) 通过 transwell 测定分析细胞侵袭和迁移生长。Ĵ通过 RT-PCR 和蛋白质印迹分析分析 E-cadherin 和 Vimentin 的表达。结果表示为三个独立实验的平均值±标准差。* P < 0.05 或 ** P < 0.01 表示指定组之间存在显着差异

全尺寸图片
图 5
图 2

YTHDF1 促进的 YAP mRNA 翻译受 m6A 修饰和与 eIF3a 相互作用的调节。a YTHDF1 的 mRNA 和蛋白质水平通过 RT-PCR 和蛋白质印迹测定在配对的新鲜 NSCLC 肿瘤癌组织(肿瘤)和匹配的相邻正常组织(正常)中进行分析(左图,n = 10;右图,n = 30 )。b通过IHC法分析YTHDF1在不同级别肺癌组织中的表达。c YTHDF1 的高表达与 NSCLC 患者较差的预后相关(P = 0.018)。(d,e)用指定的 YTHDF1 基因转染 A549 细胞。d通过划痕法分析迁移生长。e通过蛋白质印迹法分析E-钙粘蛋白和波形蛋白的表达。f异种移植肿瘤(左图)和转移性肺肿瘤(右图)源自 A549 细胞,通过皮下注射构建的指示基因稳定表达。g通过 WB 测定分析 A549 细胞中 YAP、CTGF 和 Cyr61 的蛋白质水平。h Co-IP 使用从 A549 细胞收集的裂解物进行,并通过 YTHDF1 或 eIF3a 抗体进行免疫沉淀。(ik) 在用指定基因转染嘌呤霉素处理的 A549 细胞中通过 ELISA 测定分析 YAP 的蛋白质水平。(lp)用指定的 YTHDF1 和 YAP 基因转染 A549 细胞。l通过蛋白质印迹法分析 YTHDF1、YAP、CTGF 和 Cyr61 的蛋白质水平。m通过菌落形成测定分析结肠的大小和数量。n采用transwell法分析细胞侵袭和迁移生长情况。o通过 qPCR 分析分析 E-cadherin 和 Vimentin 的表达。p通过蛋白质印迹分析分析切割的 Caspas-3 的相关性。结果表示为三个独立实验的平均值±标准差。* P < 0.05 或 ** P < 0.01 表示指定组之间存在显着差异。ns,不显着

全尺寸图片

图 1b:用于显示 ALKBH5 肿瘤组表达的错误图像(右下图);现在使用正确的图像。

图 5 h:YTHDF1 波段使用了不正确的图像;现在使用正确的波段。

此处给出了更正的数字。更正对论文的最终结论没有任何影响。原文章已更正。

  1. 金D,郭J,吴Y,等。m6A 去甲基化酶 ALKBH5 通过降低 YTHDFs 介导的 YAP 表达和抑制 miR-107/LATS2 介导的 NSCLC 中的 YAP 活性来抑制肿瘤生长和转移。摩尔癌症。2020;19:40。https://doi.org/10.1186/s12943-020-01161-1。

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  1. 金丹和郭继伟对这项工作做出了同等贡献。

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  1. 滨州医科大学附属医院临床医学检验科,滨州 256603

    金丹

  2. 滨州医科大学附属医院肿瘤研究所,滨州 256603

    Jiwei Guo, Yan Wu, Lijuan Yang, Jing Du, Juanjuan Dai, Weiwei Chen, Kaikai Gong, Shuang Miao & 李雪琳

  3. 滨州医科大学附属医院甲状腺乳腺外科,滨州 256603

    王晓红

  4. 滨州医科大学附属医院生殖医学科,滨州 256603

    孙红良

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Jin, D., Guo, J., Wu, Y.等。更正:m6A 去甲基化酶 ALKBH5 通过降低 YTHDFs 介导的 YAP 表达和抑制 miR-107/LATS2 介导的 NSCLC 中的 YAP 活性来抑制肿瘤生长和转移。摩尔癌症 21, 130 (2022)。https://doi.org/10.1186/s12943-022-01593-x

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