The role of AGR2 and AGR3 in cancer: Similar but not identical

Obacz, Joanna; Takáčová, Martina; Brychtová, Veronika; Dobeš, Petr; Pastoreková, Silvia; Vojtěšek, Bořivoj; Hrstka, Roman

doi:10.1016/j.ejcb.2015.01.002

Cited by 41 publications

(50 citation statements)

References 97 publications

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“…Moreover, although ID2 has been previously associated with EMT and shown to suppress the SMAD pathway [39][40][41], decreasing of ID2 expression by TGF-b1 stimulation was confirmed by RNA-Seq and real-time RT-PCR in the present study. Previously, a role for AGR2 in EMT was investigated [42][43][44]. We also confirmed that AGR2 expression was down-regulated by TGF-b1.…”

Section: Discussionsupporting

confidence: 82%

Regulation of Gene Expression by Sodium Valproate in Epithelial-to-Mesenchymal Transition

Noguchi

Eitoku

Moriya

et al. 2015

Lung

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Section: Discussionsupporting

confidence: 82%

Regulation of Gene Expression by Sodium Valproate in Epithelial-to-Mesenchymal Transition

Noguchi

Eitoku

Moriya

et al. 2015

Lung

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“…However, in amphibians, the nerve-derived proregenerative factor is thought to be anterior gradient protein (Ag1) (Kumar et al, 2007). Ag1 does not exist in mammals, but there are two other mammalian family members, Agr2 and Agr3 (Ivanova et al, 2013), which have been implicated in cancer, but not tissue repair (Obacz et al, 2015). Consistent with this, we have found no evidence for expression of Agr2 or Agr3 mRNAs in SCPs (data not shown).…”

Section: Discussionsupporting

confidence: 56%

Dedifferentiated Schwann Cell Precursors Secreting Paracrine Factors Are Required for Regeneration of the Mammalian Digit Tip

et al. 2016

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Adult mammals have lost multi-tissue regenerative capacity, except for the distal digit, which is able to regenerate via mechanisms that remain largely unknown. Here, we show that, after adult mouse distal digit removal, nerve-associated Schwann cell precursors (SCPs) dedifferentiate and secrete growth factors that promote expansion of the blastema and digit regeneration. When SCPs were dysregulated or ablated, mesenchymal precursor proliferation in the blastema was decreased and nail and bone regeneration were impaired. Transplantation of exogenous SCPs rescued these regeneration defects. We found that SCPs secrete factors that promote self-renewal of mesenchymal precursors, and we used transcriptomic and proteomic analysis to define candidate factors. Two of these, oncostatin M (OSM) and platelet-derived growth factor AA (PDGF-AA), are made by SCPs in the regenerating digit and rescued the deficits in regeneration caused by loss of SCPs. As all peripheral tissues contain nerves, these results could have broad implications for mammalian tissue repair and regeneration.

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“…In addition, some scholars have found that AGR2 is highly expressed in Barrett's esophageal metaplasia and esophageal adenocarcinoma . In addition to precancerous lesions of pancreatic cancer and esophageal adenocarcinoma, AGR2 is also highly expressed in breast cancer, prostate cancer, ovarian cancer, and pancreatic cancer, and involved in the process of tumor cell proliferation and metastasis . These studies indicate that AGR2 acts as an oncogene and plays an important role in the progression of various malignancies.…”

Section: Discussionmentioning

confidence: 90%

TP53 mediated miR‐3647‐5p prevents progression of cervical carcinoma by targeting AGR2

et al. 2019

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Previous studies have shown that miRNAs involved in a number of biological processes, such as cell growth, development, differentiation, and apoptosis. The dysregulation of miRNA expression is associated with various diseases, including cervical cancer. However, the involvement of miR‐3647‐5p in the progression of tumors is unclear. In this study, we confirmed that miR‐3647‐5p was down‐regulated during cervical carcinogenesis and development, which was positively correlated with the prognosis of patients with cervical cancer. In addition, our study showed that miR‐3647‐5p can inhibit the proliferation of cervical cancer cells and promote apoptosis, suggesting that miR‐3647‐5p is involved in the development of cervical cancer as a tumor suppressor gene. Furthermore, we found that transcription factor TP53 could promote the expression of miR‐3647‐5p, suggesting that the dysfunction of miR‐3647‐5p in cervical cancer may be related to TP53. In addition, we also found that miR‐3647‐5p can inhibit the proliferation of cervical cancer cells and promote apoptosis by targeting AGR2. In summary, our research reveals that transcription factor TP53 promotes the expression of miR‐3647‐5p, while up‐regulated miR‐3647‐5p targets AGR2, inhibiting cervical cancer cell proliferation and promoting apoptosis. Our study reveals the mechanism of TP53/miR‐3647‐5p/AGR2 axis in cervical cancer, which may be useful for targeted therapy of cervical cancer.

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The role of AGR2 and AGR3 in cancer: Similar but not identical

Cited by 41 publications

References 97 publications

Regulation of Gene Expression by Sodium Valproate in Epithelial-to-Mesenchymal Transition

Regulation of Gene Expression by Sodium Valproate in Epithelial-to-Mesenchymal Transition

Dedifferentiated Schwann Cell Precursors Secreting Paracrine Factors Are Required for Regeneration of the Mammalian Digit Tip

TP53 mediated miR‐3647‐5p prevents progression of cervical carcinoma by targeting AGR2

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