Lin28 promotes dental pulp cell proliferation via upregulation of cyclin-dependent proteins and interaction with let-7a/IGF2BP2 pathways

Liu, Yan; Dong, Ning; Miao, Jiyu; Li, Chenxing; Wang, Xiaofei; Ruan, Jianping

doi:10.1016/j.biopha.2019.108742

Cited by 10 publications

(16 citation statements)

References 55 publications

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“…In glioma cells, the Lin28A/SNHG14/IRF6 axis is pivotal for the reprogramming of glucose metabolism and the spurring of oncogenesis, and depletion of Lin28A reduced in vivo xenograft tumor outgrowth and prolonged nude mice survival (42). Several studies (23)(24)(25)(26) have also revealed the underlying role of LIN28A on cell cycle-related mRNAs. For instance, tissue microarrays identified that LIN28A expression was increased in epithelial tumors and promoted cell cycle progression by regulating CDK2, CCND1, and CDC25A in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…RNA binding proteins (RBPs) are key modulators of cancers and mRNAs (21,22). Previous studies have explored the effect and molecular mechanisms of the RBPs LIN28A in the development of various tumors and revealed the underlying role of LIN28A on cell cycle-related mRNAs (23)(24)(25)(26). Lin28 has been found to enhance the growth of dental pulp cells by upregulating the cyclin-dependent proteins and by interacting with the let-7a/IGF2BP2 pathway (23).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have explored the effect and molecular mechanisms of the RBPs LIN28A in the development of various tumors and revealed the underlying role of LIN28A on cell cycle-related mRNAs (23)(24)(25)(26). Lin28 has been found to enhance the growth of dental pulp cells by upregulating the cyclin-dependent proteins and by interacting with the let-7a/IGF2BP2 pathway (23). In epithelial tumors, LIN28A promoted cell cycle procession by moderating the expression of CDK2, Cyclin D1, and CDC25A (26).…”

Section: Introductionmentioning

confidence: 99%

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Lin28A/CENPE Promoting the Proliferation and Chemoresistance of Acute Myeloid Leukemia

Shi

Niu

et al. 2021

Front. Oncol.

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The prognosis of chemoresistant acute myeloid leukemia (AML) is still poor, mainly owing to the sustained proliferation ability of leukemic cells, while the microtubules have a major role in sustaining the continuity of cell cycle. In the present study, we have identified CENPE, a microtubular kinesin-like motor protein that is highly expressed in the peripheral blood of patients with chemoresistant AML. In our in vitro studies, knockdown of CENPE expression resulted in the suppression of proliferation of myeloid leukemia cells and reversal of cytarabine (Ara-C) chemoresistance. Furthermore, Lin28A, one of the RNA-binding oncogene proteins that increase cell proliferation and invasion and contribute to unfavorable treatment responses in certain malignancies, was found to be remarkably correlated with CENPE expression in chemoresistance AML. Overexpression of LIN28A promoted the proliferation and Ara-C chemoresistance of leukemic cells. RIP assay, RNA pull-down, and dual luciferase reporter analyses indicated that LIN28A bound specifically to the promoter region GGAGA of CENPE. In addition, the impacts of LIN28A on cell growth, apoptosis, cell cycle progression, and Ara-C chemoresistance were reverted by the knockdown of CENPE. Hence, Lin28A/CENPE has enhanced the proliferation and chemoresistance of AML, and therefore, it could be a prospective candidate for AML treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lin28A/CENPE Promoting the Proliferation and Chemoresistance of Acute Myeloid Leukemia

Shi

Niu

et al. 2021

Front. Oncol.

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“… 46 , 47 IGF2BP proteins have been ascribed an “anti-apoptotic role” in multiple cell contexts, 48 , 49 , 50 and IGF2BP is known to boost proliferation of several tissues. 51 , 52 , 53 Thus, upregulated IGF2BP2 may explain our observed increased survival and proliferation of hematopoietic stem and progenitor cells (HSPCs). Alternatively, HMGA2 binds the DNA replication fork in murine embryonic stem cells and protects against nucleolytic fork collapse, which can cause double strand DNA breaks and trigger apoptosis, a differentiation block, or senescence.…”

Section: Discussionmentioning

confidence: 88%

3’ UTR-truncated HMGA2 overexpression induces non-malignant in vivo expansion of hematopoietic stem cells in non-human primates

Bonner

Morales-Hernández

Zhou

et al. 2021

Molecular Therapy - Methods & Clinical Development

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Vector-mediated mutagenesis remains a major safety concern for many gene therapy clinical protocols. Indeed, lentiviral-based gene therapy treatments of hematologic disease can result in oligoclonal blood reconstitution in the transduced cell graft. Specifically, clonal expansion of hematopoietic stem cells (HSCs) highly expressing HMGA2, a chromatin architectural factor found in many human cancers, is reported in patients undergoing gene therapy for hematologic diseases, raising concerns about the safety of these integrations. Here, we show for the first time in vivo multilineage and multiclonal expansion of non-human primate HSCs expressing a 3’ UTR-truncated version of HMGA2 without evidence of any hematologic malignancy >7 years post-transplantation, which is significantly longer than most non-human gene therapy pre-clinical studies. This expansion is accompanied by an increase in HSC survival, cell cycle activation of downstream progenitors, and changes in gene expression led by the upregulation of IGF2BP2 , a mRNA binding regulator of survival and proliferation. Thus, we conclude that prolonged ectopic expression of HMGA2 in hematopoietic progenitors is not sufficient to drive hematologic malignancy and is not an acute safety concern in lentiviral-based gene therapy clinical protocols.

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“…Consistent with the above report, this study also identified the pro-migratory function of IGF2BP2 in keratinocytes. Furthermore, IGF2BP2 exhibited pro-proliferation role in dental pulp cells and colorectal cancer cells [ 31 , 32 ]. Here, we firstly validated IGF2BP2 knockdown repressed keratinocyte proliferation.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor 2 mRNA binding protein 2 regulates proliferation, migration, and angiogenesis of keratinocytes by modulating heparanase stability

Zhi¹,

Li²,

Kong³

et al. 2021

Bioengineered

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Wound healing is related to proliferation, migration, and angiogenesis of keratinocytes. Insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) is an important N6-methyladenosine (m6A) reader, which is involved in multiple processes, including wound healing. However, the function and mechanism of IGF2BP2 in keratinocyte processes are largely uncertain. In the present study, expression levels of IGF2BP2 and heparanase (HPSE) were detected by quantitative reverse transcription polymerase chain reaction and western blotting assays. Cell proliferation was investigated by cell counting kit-8 (CCK-8) analysis. Cell migration was determined through wound healing assay. Angiogenesis was measured by tube formation assay and vascular endothelial growth factor (VEGF) level using enzyme linked immunosorbent assay (ELISA). The interaction between IGF2BP2 and HPSE was analyzed by RNA immunoprecipitation, pull-down and luciferase reporter analyses. The results showed that IGF2BP2 expression was enhanced in wound healing. IGF2BP2 downregulation constrained HaCaT cell proliferation, migration, and angiogenesis. IGF2BP2 knockdown decreased HPSE expression. IGF2BP2 could regulate HPSE stability by binding with 3ʹ untranslated region (UTR) of HPSE. HPSE upregulation attenuated silencing IGF2BP2-mediated suppression of proliferation, migration, and angiogenesis. As a conclusion, IGF2BP2 knockdown repressed proliferation, migration, and angiogenesis of HaCaT cells by decreasing HPSE stability.

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Lin28 promotes dental pulp cell proliferation via upregulation of cyclin-dependent proteins and interaction with let-7a/IGF2BP2 pathways

Cited by 10 publications

References 55 publications

Lin28A/CENPE Promoting the Proliferation and Chemoresistance of Acute Myeloid Leukemia

Lin28A/CENPE Promoting the Proliferation and Chemoresistance of Acute Myeloid Leukemia

3’ UTR-truncated HMGA2 overexpression induces non-malignant in vivo expansion of hematopoietic stem cells in non-human primates

Insulin-like growth factor 2 mRNA binding protein 2 regulates proliferation, migration, and angiogenesis of keratinocytes by modulating heparanase stability

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