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Correction: PTENP1/miR-20a/PTEN axis contributes to breast cancer progression by regulating PTEN via PI3K/AKT pathway

The Original Article was published on 13 June 2019

Correction: J Exp Clin Cancer Res 38, 256 (2019)

Following publication of the original article [1], the authors identified an errors in the images of Figs. 3 and 6, specifically:

  • Fig. 3E – Migration, group of siSCR

  • Fig. 6D – T47D, group of anti-miR-NC + siPTENP1

  • Fig. 6E – Migration, group of anti-miR-20a + siSCR

The correct figures are given below.

Fig. 3
figure 1

Low PTENP1 level enhances the malignant behavior of BC cells. a The viability of transfected BC cells were detected by CCK8 assays at 0, 24, 48,72, 96 h. b Knockdown of PTENP1 enhanced the colony formation in BC cells. c The proliferation of siPTENP1 transfected cells was increased by Edu staining (Scale bar = 20 μm). d Ki67 staining also showed intensive proliferation (Scale bar = 20 μm). e The aggressiveness was enhanced with knocking down PTENP1 in MCF-7 cells (Scale bar = 20 μm). f The siPTENP1-MCF-7 cells revealed more resistance to ADR. g Higher IC50 value was also proved the enhanced chemoresistance to ADR. h Weakened colony formation ability was shown in response to ADR. i More resistance to ADR was shown in siPTENP1-MCF-7 cells. Low apoptosis rate was detected by flow cytometry. j JC-1 staining assay showed altered mitochondrial membrane potential with siPTENP1 transfection. Green fluorescence: the monomer, red fluorescence: the J-aggregates, orange fluorescence: merged photo (Scale bar = 20 μm). k TUNEL assay confirmed the incidence of apoptosis (Scale bar = 200 μm). l Apoptosis-related molecules expression was determined by western blot. m The xenografted tumors were presented with or without ADR treatment. n PTEN and Ki67 levels were determined by IHC staining. Data are the means ± SD of triplicate determinants (*P < 0.05) (Scale bar = 200 μm)

Fig. 6
figure 2

Inhibition of miR-20a reverses the promotional effect of siPTENP1 by mediating PTEN expression in BC progression. a PTEN mRNA expression was identified with the treatment of miR-20a inhibitor or siPTENP1. b PTEN protein level was detected by western blot. c The proliferation was measured by CCK8 assays. d Colony formation assay was used to measure the colony formation of transfected cells. e The aggressiveness was determined by transwell assay (Scale bar = 20 μm). f CCK8 assays were carried out to assess the chemoresistance to ADR with different treated BC cells. g IC50 values were calculated in differential treated MCF-7 cells. h In response to ADR, the colony formation was measured in transfected MCF-7 cells. i The AnnexinV and PI staining was used to determine the occurrence of apoptosis. Data are means ± SD of three independent assays (*P < 0.05)


  1. Gao X, Qin T, Mao J, et al. PTENP1/miR-20a/PTEN axis contributes to breast cancer progression by regulating PTEN via PI3K/AKT pathway. J Exp Clin Cancer Res. 2019;38:256.

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Correspondence to Lianhong Li.

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Gao, X., Qin, T., Mao, J. et al. Correction: PTENP1/miR-20a/PTEN axis contributes to breast cancer progression by regulating PTEN via PI3K/AKT pathway. J Exp Clin Cancer Res 42, 202 (2023).

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