Pinin Induces Epithelial-to-Mesenchymal Transition in Hepatocellular Carcinoma by Regulating m6A Modification

Qiao, Kun; Chen, Caihong; Liu, Haoyang; Qin, Yuan; Liu, Huijuan

doi:10.1155/2021/7529164

Cited by 7 publications

(6 citation statements)

References 35 publications

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“… 77 Qiao et al. 273 reported pinin, a protein localizes to desmosomes and nucleus, formed condensates with METTL3 then suppressed by 1,6‐hexanediol. Moreover, 1,6‐hexanediol prevents phase separation of SARS2‐NP, IDR‐rich scaffold protein NSP5, RNA chaperone NSP2, BRD4, and MED1 effectively.…”

Section: Regulatory Targets and Methods Of Biomolecular Condensatesmentioning

confidence: 99%

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Biomolecular condensates: Formation mechanisms, biological functions, and therapeutic targets

Niu

Zhang

et al. 2023

MedComm

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Biomolecular condensates are cellular structures composed of membraneless assemblies comprising proteins or nucleic acids. The formation of these condensates requires components to change from a state of solubility separation from the surrounding environment by undergoing phase transition and condensation. Over the past decade, it has become widely appreciated that biomolecular condensates are ubiquitous in eukaryotic cells and play a vital role in physiological and pathological processes. These condensates may provide promising targets for the clinic research. Recently, a series of pathological and physiological processes have been found associated with the dysfunction of condensates, and a range of targets and methods have been demonstrated to modulate the formation of these condensates. A more extensive description of biomolecular condensates is urgently needed for the development of novel therapies. In this review, we summarized the current understanding of biomolecular condensates and the molecular mechanisms of their formation. Moreover, we reviewed the functions of condensates and therapeutic targets for diseases. We further highlighted the available regulatory targets and methods, discussed the significance and challenges of targeting these condensates. Reviewing the latest developments in biomolecular condensate research could be essential in translating our current knowledge on the use of condensates for clinical therapeutic strategies.

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Section: Regulatory Targets and Methods Of Biomolecular Condensatesmentioning

confidence: 99%

“…1,6‐Hexanediol inhibits phase separation of architectural long noncoding RNA NEAT1 and prevents assembly process of paraspeckles 77 . Qiao et al 273 . reported pinin, a protein localizes to desmosomes and nucleus, formed condensates with METTL3 then suppressed by 1,6‐hexanediol.…”

Section: Regulatory Targets and Methods Of Biomolecular Condensatesmentioning

confidence: 99%

Biomolecular condensates: Formation mechanisms, biological functions, and therapeutic targets

Niu

Zhang

et al. 2023

MedComm

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“…Epithelial-mesenchymal transition (EMT) refers to how epithelial cells are depolarized and transformed into mesenchymal cells due to certain factors ( Jiang et al, 2022 ). During the metastasis in epithelial tumors, the phenotype of tumor cells changes primarily caused by environmental stimuli that enable tumor cells to adapt to the various microenvironments they encounter (intercellular stroma, humoral components, or blood) ( Park et al, 2020 ; Qiao et al, 2021 ). EMT regulates these phenotypic transformations.…”

Section: Introductionmentioning

confidence: 99%

Puerarin inhibits EMT induced by oxaliplatin via targeting carbonic anhydrase XII

Chen

Zhou²,

Zhang³

et al. 2022

Front. Pharmacol.

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Puerarin is a flavonoid molecule that widely exists in various plants. Puerarin has been reported to exhibit anti-tumor effects in various cancers. However, its exact underlying pharmacological mechanism is unclear. This study evaluated the anticancer effect of puerarin combined with oxaliplatin (OXA) in vitro and in vivo. Our results indicated that puerarin can reverse platinum-based anti-cancer drug resistance, and enhance the OXA’s anticancer effects on breast cancer. Furthermore, puerarin can inhibit migration and reverse the epithelial-mesenchymal transition (EMT) induced by low-dose OXA. Further studies showed that the carbonic anhydrase (CA) XII is a potential target of puerarin. In conclusion, puerarin is expected to become an adjuvant chemotherapy drug and potentially become one of the medicated foods for breast cancer patients.

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“…Exosomes have been proposed as a therapeutic tool to control the development of EMT and influence the progression of cancer[ 10 ]. In addition, Pinin induces EMT and malignant progression in hepatocellular carcinoma[ 11 ]. Furthermore, Wu et al [ 12 ] found that interleukin (IL)-6 secreted by cancer-associated fibroblasts promotes EMT and GC metastasis through the JAK2/STAT3 signaling pathway, Li et al [ 13 ] reported that tumor-associated neutrophils induce EMT by IL-17a to promote migration and invasion in GC cells, and Tian et al [ 14 ] reported that SERPINH1 regulates EMT and GC metastasis through the Wnt/β-catenin signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-34 promotes the proliferation and epithelial-mesenchymal transition of gastric cancer cells

Li¹,

Chen²,

Chen³

et al. 2022

World J Gastrointest Oncol

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BACKGROUND Interleukin (IL)-34 is a pro-inflammatory cytokine involved in tumor development. The role of IL-34 in the proliferation and epithelial-mesenchymal transition (EMT) of gastric cancer (GC) remains to be investigated. AIM To investigate whether and how IL-34 affects the proliferation of GC cells and EMT. METHODS Using immunohistochemical staining, the expression of IL-34 protein was detected in 60 paired GC and normal paracancerous tissues and the relationship between IL-34 and clinicopathological factors was analyzed. The expression of IL-34 mRNA and protein in normal gastric epithelial cell lines and GC was detected using quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting, respectively. Stable IL-34 knockdown and overexpression in AGS cell lines were established by lentiviral infection and validated by qRT-PCR and western blotting. The cholecystokinin-8 assay, clone formation assay, cell scratch assay, and transwell system were used to detect GC cell proliferation, clone formation, migration, and invasion capacity, respectively. The effects of IL-34 on the growth of GC transplant tumors were assessed using a subcutaneous transplant tumor assay in nude mice. The effects of IL-34 on the expression level of EMT-associated proteins in AGS cells were examined by western blotting. RESULTS Expression of IL-34 protein and mRNA was higher in GC cell lines than in GES-1 cells. Compared to matched normal paraneoplastic tissues, the expression of IL-34 protein was higher in 60 GC tissues, which was correlated with tumor size, T-stage, N-stage, tumor, node and metastasis stage, and degree of differentiation. Knockdown of IL-34 expression inhibited the proliferation, clone formation, migration, and invasion of AGS cells, while overexpression of IL-34 promoted cell proliferation, clone formation, migration, and invasion. Furthermore, the reduction of IL-34 promoted the expression of E-cadherin in AGS cells but inhibited the expression of vimentin and N-cadherin. Overexpression of IL-34 inhibited E-cadherin expression but promoted expression of vimentin and N-cadherin in AGS cells. Overexpression of IL-34 promoted the growth of subcutaneous transplanted tumors in nude mice. CONCLUSION IL-34 expression is increased in GC tissues and cell lines compared to normal gastric tissues or cell lines. In GC cells, IL-34 promoted proliferation, clone formation, migration, and invasion by regulating EMT-related protein expression cells. Interference with IL-34 may represent a novel strategy for diagnosis and targeted therapy of GC.

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Pinin Induces Epithelial-to-Mesenchymal Transition in Hepatocellular Carcinoma by Regulating m6A Modification

Cited by 7 publications

References 35 publications

Biomolecular condensates: Formation mechanisms, biological functions, and therapeutic targets

Biomolecular condensates: Formation mechanisms, biological functions, and therapeutic targets

Puerarin inhibits EMT induced by oxaliplatin via targeting carbonic anhydrase XII

Interleukin-34 promotes the proliferation and epithelial-mesenchymal transition of gastric cancer cells

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