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Correction: miR-29c plays a suppressive role in breast cancer by targeting the TIMP3/STAT1/FOXO1 pathway

Clinical Epigenetics volume 14, Article number: 97 (2022) Cite this article

The Original Article was published on 16 May 2018

Correction: Clinical Epigenetics (2018) 10:64 https://doi.org/10.1186/s13148-018-0495-y

Following publication of the original article [1], the authors noticed the errors in Fig. 4b and Fig. S4A in the supplementary material. The revised Fig. 4 has been presented with this erratum and the revised supplementary material with the inclusion of new Fig. S4A has been uploaded.

Fig. 4
figure 4

miR-29c inhibited the proliferation, migration and invasion, colony formation, and growth in 3D Matrigel of breast cancer cells. a Proliferation ofMCF-7 anti-miR-29c is higher than that of MCF-7 Cntl by CCK8 proliferation assay. b Migration and invasion of MCF-7 anti-miR-29cis higher than that ofMCF-7 Cntl. c Proliferation of MDA-MB-231 miR-29c mimic is lower than that MDA-MB-231 Cntl by CCK8 proliferation assay. d Migration and invasion assays of MDA-MB-231 miR-29c mimic are lower than that MDA-MB-231 Cntl. e Colony formations of MCF-7 anti-miR-29c are more than that of MCF-7Cntl in Soft agar assays. f Growth of MCF-7 anti-miR-29c is more than that of MCF-7 Cntl in 3D Matrigel culture. g Colony formations of MDA-MB-231miR-29c mimic are less than that of MDA-MB-231 Cntl in soft agar assays. h Growth of MDA-MB-231 miR-29c mimic is less than that of MDA-MB-231Cntl in 3D Matrigel culture. Data are presented as mean ± SD from three independent experiments, and every experiment was repeated three times, *P < 0.05

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Reference

  1. Li W, et al. miR-29c plays a suppressive role in breastcancer by targeting the TIMP3/STAT1/FOXO1 pathway. Clin Epigenet. 2018;10:64. https://doi.org/10.1186/s13148-018-0495-y.

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  1. Wan Li and Jie Yi contributed equally to this work.

Authors and Affiliations

  1. The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China

    Wan Li, Xiangjin Zheng, Weiqi Fu, Liwen Ren, Jinhua Wang & Guanhua Du

  2. Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100050, China

    Wan Li, Xiangjin Zheng, Weiqi Fu, Liwen Ren, Li Li, Jinhua Wang & Guanhua Du

  3. Department of Clinical Laboratory, Peking Union Medical College Hospital, Beijing, 100730, China

    Jie Yi

  4. Department of Endocrinology, Shanxi DAYI Hospital, Shanxi Medical University, Taiyuan, 030002, Shanxi, China

    Shiwei Liu

  5. Department of Translational Molecular Medicine, John Wayne Cancer Institute (JWCI) at Providence Saint John’s Health Center, Santa Monica, CA, 90404, USA

    Dave S. B. Hoon

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  1. Wan Li
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  2. Jie Yi
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Correspondence to Jinhua Wang or Guanhua Du.

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Supplementary Information

Additional file 1: Table S1.

Sequence of DNMT3B siRNA. Table S2. Primers of miR-29c and DNMT3B. Table S3. Primers of TIMP3 for methylation specific PCR and unmethylation PCR. Figure S1. Quantification of protein expression level of DNMT3B in human breastcancer tissues and the paired adjacent non-tumor tissues. Figure S2. Migration and invasion of cells. Figure S3. miR-29c inhibited proliferation, migration and invasion, colony formation and growth in 3D Matrigel of MDA-MB-436 cells. Figure S4. DNMT3B promoted migration, invasion, colony formation and growth in 3D Matrigel of MDA-MB-231 miR-29c cells. Figure S5. Colony formation of cells. Figure S6. miR-29c reduced luciferase activity of wild type 3’UTR of DNMT3B-luciferase reporter, and not the mutant type 3’UTR of DNMT3B reporter in MCF-7 cells. Figure S7. Expression of DNMT3B, TIMP3, STAT1 and FOXO1. Figure S8. Migration and invasion of cells.

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Li, W., Yi, J., Zheng, X. et al. Correction: miR-29c plays a suppressive role in breast cancer by targeting the TIMP3/STAT1/FOXO1 pathway. Clin Epigenet 14, 97 (2022). https://doi.org/10.1186/s13148-022-01317-4

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  • DOI: https://doi.org/10.1186/s13148-022-01317-4

Clinical Epigenetics

ISSN: 1868-7083

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