Steroid 5α-Reductase Type I Induces Cell Viability and Migration via Nuclear Factor-κB/Vascular Endothelial Growth Factor Signaling Pathway in Colorectal Cancer

Wei, Rongfang; Zhong, Sixia; Qiao, Li; Guo, Mengjie; Shao, Miaomiao; Wang, Suyu; Jiang, Bin; Yang, Ye; Gu, Chunyan

doi:10.3389/fonc.2020.01501

Cited by 15 publications

(13 citation statements)

References 49 publications

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“…Flow cytometry (Merck Millipore, Darmstadt, Germany) was applied to detect cell cycle and apoptosis, and the methods were performed as described previously. 17 …”

Section: Methodsmentioning

confidence: 99%

Splicing factor arginine/serine‐rich 8 promotes multiple myeloma malignancy and bone lesion through alternative splicing of CACYBP and exosome‐based cellular communication

Zhang

Sun

et al. 2022

Clinical & Translational Med

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Background Multiple myeloma (MM) is a distinctive malignancy of plasma cell within the bone marrow (BM), of which alternative splicing factors play vital roles in the progression. Splicing factor arginine/serine‐rich 8 (SFRS8) is the exclusive factor associated with MM prognosis, however its role in MM remains undefined. Methods The analyses of 3‐(4,5)‐dimethylthiahiazo (‐z‐y1)‐3,5‐di‐ phenytetrazoliumromide (MTT) assay, immunohistochemistry, flow cytometry and xenograft model were performed to examine cell proliferation, cell cycle and apoptosis in SFRS8 overexpression or knockdown MM cells in vitro and in vivo. The SFRS8‐regulated alternative splicing events were identified by RNA immunoprecipitation sequencing (RIP‐seq) and validated by RIP‐qPCR and Co‐IP methods. Exosomes were extracted from the supernatant of myeloma cells by ultracentrifugation. Bone lesion was evaluated by TRAP staining in vitro and SCID/NOD‐TIBIA mouse model. A neon electroporation system was utilised to deliver siRNA through exosomes. The effect of siRNA‐loaded exosomes in vivo was evaluated by using a patient‐derived tumor xenograft (PDX) model and SCID/NOD‐TIBIA mouse model. Results SFRS8 was significantly upregulated in MM samples and positively associated with poor overall survival (OS) in MM patients. SFRS8 promoted MM cell proliferation in vitro and in vivo. Furthermore, calcyclin binding protein (CACYBP) was identified as the downstream target of SFRS8. Particularly, SFRS8 could reduce CACYBP isoform1 (NM_014412.3) and increase CACYBP isoform2 (NM_001007214.1) by mediating the alternative splicing of CACYBP, thereby altering the ubiquitination degradation of β‐catenin to promote MM progression. In addition, SFRS8 promoted osteoclast differentiation through exosomes in vitro and in vivo. More importantly, exosomal siRNA targeting CACYBP isoform2 inhibited tumour growth in PDX and SCID/NOD‐TIBIA mouse models. Conclusion Our findings demonstrate that targeting the SFRS8/CACYBP/β‐catenin axis may be a promising strategy for MM diagnosis and treatment.

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“…Flow cytometry (Merck Millipore, Darmstadt, Germany) was applied to detect cell cycle and apoptosis, and the methods were performed as described previously. 17 …”

Section: Methodsmentioning

confidence: 99%

Splicing factor arginine/serine‐rich 8 promotes multiple myeloma malignancy and bone lesion through alternative splicing of CACYBP and exosome‐based cellular communication

Zhang

Sun

et al. 2022

Clinical & Translational Med

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“…Cell cycle and apoptosis were performed according to previous report ( 15 ) and analyzed by flow cytometry (Merck Millipore, Germany).…”

Section: Methodsmentioning

confidence: 99%

NAT10 acetylates BCL-XL mRNA to promote the proliferation of multiple myeloma cells through PI3K-AKT pathway

et al. 2022

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Multiple myeloma (MM) is a clinically distinctive plasma cell malignancy in the bone marrow (BM), in which epigenetic abnormalities are featured prominently. Epigenetic modifications including acetylation have been deemed to contribute to tumorigenesis. N-acetyltransferase 10 (NAT10) is an important regulator of mRNA acetylation in many cancers, however its function in MM is poorly studied. We first analyzed MM clinical databases and found that elevated NAT10 expression conferred a poor prognosis in MM patients. Furthermore, overexpression of NAT10 promoted MM cell proliferation. The correlation analysis of acRIP-seq screened BCL-XL (BCL2L1) as a significant downstream target of NAT10. Further RNA decay assay showed that increased NAT10 improved the stability of BCL-XL mRNA and promoted protein translation to suppress cell apoptosis. NAT10 activated PI3K-AKT pathway and upregulated CDK4/CDK6 to accelerate cellular proliferation. Importantly, inhibition of NAT10 by Remodelin suppressed MM cell growth and induced cell apoptosis. Our findings show the important role of NAT10/BCL-XL axis in promoting MM cell proliferation. Further explorations are needed to fully define the potential of targeting NAT10 therapy in MM treatment.

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“…IHC examination was performed as described previously [42]. The posterior superior iliac spine of MM patients was chosen as the biopsy point.…”

Section: Methodsmentioning

confidence: 99%

AIMP1 promotes multiple myeloma malignancy through interacting with ANP32A to mediate histone H3 acetylation

Wei

Zhu

Zhang

et al. 2022

Cancer Communications

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Background: Multiple myeloma (MM) is the second most common hematological malignancy. An overwhelming majority of patients with MM progress to serious osteolytic bone disease. Aminoacyl-tRNA synthetase-interacting multifunctional protein 1 (AIMP1) participates in several steps during cancer development and osteoclast differentiation. This study aimed to explore its role in MM. Methods: The gene expression profiling cohorts of MM were applied to determine the expression of AIMP1 and its association with MM patient prognosis. Enzyme-linked immunosorbent assay, immunohistochemistry, and Western blotting were used to detect AIMP1 expression. Protein chip

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Steroid 5α-Reductase Type I Induces Cell Viability and Migration via Nuclear Factor-κB/Vascular Endothelial Growth Factor Signaling Pathway in Colorectal Cancer

Cited by 15 publications

References 49 publications

Splicing factor arginine/serine‐rich 8 promotes multiple myeloma malignancy and bone lesion through alternative splicing of CACYBP and exosome‐based cellular communication

Splicing factor arginine/serine‐rich 8 promotes multiple myeloma malignancy and bone lesion through alternative splicing of CACYBP and exosome‐based cellular communication

NAT10 acetylates BCL-XL mRNA to promote the proliferation of multiple myeloma cells through PI3K-AKT pathway

AIMP1 promotes multiple myeloma malignancy through interacting with ANP32A to mediate histone H3 acetylation

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