Correction to: Knockdown of FOXO3a induces epithelial-mesenchymal transition and promotes metastasis of pancreatic ductal adenocarcinoma by activation of the β-catenin/TCF4 pathway through SPRY2

Li, Jun; Yang, Rumeng; Dong, Yuting; Chen, Manyao; Wang, Yu; Wang, Guoping

doi:10.1186/s13046-021-02033-2

Cited by 5 publications

(8 citation statements)

References 1 publication

(1 reference statement)

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“…The Editor-in-Chief has retracted this article. A Correction was published in 2021 [1]. Subsequently concerns have been raised with respect to both the original figures and the figures in the Correction.…”

mentioning

confidence: 99%

Retraction Note: Knockdown of FOXO3a induces epithelialmesenchymal transition and promotes metastasis of pancreatic ductal adenocarcinoma by activation of the βcatenin/TCF4 pathway through SPRY2

Yang

Dong

et al. 2022

J Exp Clin Cancer Res

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mentioning

confidence: 99%

Retraction Note: Knockdown of FOXO3a induces epithelialmesenchymal transition and promotes metastasis of pancreatic ductal adenocarcinoma by activation of the βcatenin/TCF4 pathway through SPRY2

Yang

Dong

et al. 2022

J Exp Clin Cancer Res

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“…40 However, FOXO3a can also alter the expression levels of βcatenin and TCF4 in tumor cells. 29 FOXO3a acts as a transcription factor that indirectly regulates βcatenin levels by regulating the expression of miR-34. 30 Indeed, both the mRNA and protein expression of βcatenin and TCF4 were reduced after FOXO3a knockdown in NSCs.…”

Section: Discussionmentioning

confidence: 99%

“…One study showed that changes in FOXO3a expression are followed by changes in the mRNA and protein expression levels of βcatenin and TCF4. 29 It has also been shown that FOXO3a acts as a repressor of Wnt signaling by promoting miR-34 expression to inhibit βcatenin. 30 Therefore, we speculated that the interference of FOXO3a with NSC proliferation may also be mediated by affecting the expression of βcatenin and TCF4.…”

Section: Introductionmentioning

confidence: 99%

miR‐872‐5p/FOXO3a/Wnt signaling feed‐forward loop promotes proliferation of endogenous neural stem cells after spinal cord ischemia–reperfusion injury in rats

Zhang

Cui

et al. 2023

The FASEB Journal

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The activation of endogenous neural stem cells (NSCs) is considered an important mechanism of neural repair after mechanical spinal cord injury; however, whether endogenous NSC proliferation can also occur after spinal cord ischemia–reperfusion injury (SCIRI) remains unclear. In this study, we aimed to verify the existence of endogenous NSC proliferation after SCIRI and explore the underlying molecular mechanism. NSC proliferation was observed after SCIRI in vivo and oxygen–glucose deprivation and reperfusion (OGD/R) in vitro, accompanied by a decrease in forkhead box protein O 3a (FOXO3a) expression. This downward trend was regulated by the increased expression of microRNA‐872‐5p (miR‐872‐5p). miR‐872‐5p affected NSC proliferation by targeting FOXO3a to increase the expression of β‐catenin and T‐cell factor 4 (TCF4). In addition, TCF4 in turn acted as a transcription factor to increase the expression level of miR‐872‐5p, and knockdown of FOXO3a enhanced the binding of TCF4 to the miR‐872‐5p promoter. In conclusion, SCIRI in vivo and OGD/R in vitro stimulated the miR‐872‐5p/FOXO3a/β‐catenin‐TCF4 pathway, thereby promoting NSC proliferation. At the same time, FOXO3a affected TCF4 transcription factor activity and miR‐872‐5p expression, forming a positive feedback loop that promotes NSC proliferation.

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“…FOXO1 inhibits TGFb-induced EMT, negatively regulates EMT transcription factors, and interacts with ZEB2 (32). In pancreatic ductal carcinoma, FOXO depletion induces EMT via activation of the b-catenin/transcription factor 4 (TCF4) pathway, a known CSC-associated signaling pathway (33).…”

Section: Emt Em Plasticity and Cancer Stem Cell Propertiesmentioning

confidence: 99%

Forkhead Box Transcription Factors: Double-Edged Swords in Cancer

2022

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A plethora of treatment options exist for cancer therapeutics, but many are limited by side effects and either intrinsic or acquired resistance. The need for more effective targeted cancer treatment has led to the focus on forkhead box transcription factors as possible drug targets. Forkhead factors such as FOXA1 and FOXM1 are involved in hormone regulation, immune system modulation, and disease progression through their regulation of the epithelial-mesenchymal transition. Forkhead factors can influence cancer development, progression, metastasis, and drug resistance. In this review, we discuss the various roles of forkhead factors in biological processes that support cancer as well as their function as pioneering factors and their potential as targetable transcription factors in the fight against cancer.

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Correction to: Knockdown of FOXO3a induces epithelial-mesenchymal transition and promotes metastasis of pancreatic ductal adenocarcinoma by activation of the β-catenin/TCF4 pathway through SPRY2

Cited by 5 publications

References 1 publication

Retraction Note: Knockdown of FOXO3a induces epithelialmesenchymal transition and promotes metastasis of pancreatic ductal adenocarcinoma by activation of the βcatenin/TCF4 pathway through SPRY2

Retraction Note: Knockdown of FOXO3a induces epithelialmesenchymal transition and promotes metastasis of pancreatic ductal adenocarcinoma by activation of the βcatenin/TCF4 pathway through SPRY2

miR‐872‐5p/FOXO3a/Wnt signaling feed‐forward loop promotes proliferation of endogenous neural stem cells after spinal cord ischemia–reperfusion injury in rats

Forkhead Box Transcription Factors: Double-Edged Swords in Cancer

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