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MiRNA for MACF1 regulates osteoblast differentiation

ABSTRACT: miRNA for MACF1 regulates osteoblast differentiation

PROVIDER: PRJNA837887 | ENA |

REPOSITORIES: ENA

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MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [ChIP-seq]

Project description:Osteoblast differentiation leading to bone formation requires a coordinated transcriptional program. We have recently demonstrated that microtubule actin crosslinking factor 1 (MACF1) promotes osteoblast differentiation, suggesting a key role in regulating early-phase osteoblast differentiation. Here, we showed that the early-phase osteoblast differentiation transcriptome dynamics was regulated by MACF1 and the transcription of TCF7/LEF1, key effectors of Wnt signaling that is important for osteoblast differentiation was suppressed by MACF1 knockdown. Co-IP and Protein mass spectrometry revealed that MACF1 interacted with a known and two previously unknown repressors of TCF7/LEF1, DKK1, CDK12 and MEAF6. ChIP-seq analysis of MACF1-associated promoters further revealed that MACF1 interacted with transcription factors TCF12 and E2F6, which also suppressed the transcription of TCF7/LEF1. Furthermore, all these four MACF-interacted proteins inhibited osteoblast differentiation. By studying the underlying mechanism, we found that cytoplasmic-nuclear localization of MACF1 was dependent on its level and the cytoplasmic-nuclear localization of TCF12 and E2F6 was regulated by MACF1 localization. In addition, MACF1 oppositely regulated the transcription activity of TCF12 and TCF7. Current study, for the first time to our knowledge, suggest that MACF1 acts as a sponge of osteoblast differentiation repressors to promote osteoblast differentiation, and indicate a novel mechanism for regulating the cellular location of transcription factors by a protein associated with microtubule and actin.

2021-02-17 | GSE120251 | GEO

MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [RNA-seq]

2021-02-17 | GSE120248 | GEO

miRNA for MACF1 regulates osteoblast differentiation

Project description:MC3T3-E1 cells were transfected with short hairpin RNA (shRNA) specifically targeting the murine MACF1 lentivirus vector or with scrambled shRNA, and the stably transfected cell lines were selected using puromycin. After 15 days of selection, all cells were collected for further study.

2022-10-27 | GSE202962 | GEO

MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm

Project description:MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm

| PRJNA492304 | ENA

MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [ChIP-seq]

Project description:MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [ChIP-seq]

| PRJNA492306 | ENA

MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [RNA-seq]

Project description:MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [RNA-seq]

| PRJNA492300 | ENA

Mechanical loading influences osteocytes and further regulates osteoblast metabolism and osteogenic differentiation(miRNA Array)

Project description:Mechanical loading influences osteocytes and further regulates osteoblast metabolism and osteogenic differentiation(miRNA Array)

| PRJNA742690 | ENA

RNA-seq in osteoblast differentiation

Project description:RNA-seq in osteoblast differentiation

| PRJNA705674 | ENA

Anthocyanin-treated osteoblast cells [miRNA-seq]

Project description:Anthocyanin-treated osteoblast cells [miRNA-seq]

| PRJNA826064 | ENA

MACF1 Promotes Colorectal Cancer Progression via ATF4-Mediated ASNS Regulation

Project description:Background: Microtubule-actin cross-linking factor 1 (MACF1) is a cytoskeletal cross-linker implicated in cancer pathogenesis, yet its role in colorectal cancer (CRC) progression remains unclear. This study investigated MACF1 expression, function, and its mechanistic link to the ATF4-ASNS regulatory axis in CRC. Methods: MACF1 expression was assessed in CRC tissues and cell lines (HCT116, HT29, SW620, Caco2, LoVo) via immunohistochemistry and qPCR. Functional assays—including proliferation, colony formation, wound healing, Transwell migration, and cell-cycle analysis—were performed following MACF1 knockdown and overexpression. In vivo tumor growth was evaluated using a subcutaneous xenograft model. RNA-seq screening identified ASNS as a downstream effector, and the MACF1–ATF4–ASNS relationship was explored through ChIP, immunofluorescence, nuclear fractionation, and Co-IP. Results: MACF1 was significantly elevated in CRC tissues and cells versus controls (p < 0.05). MACF1 knockdown suppressed proliferation, colony formation, migration, and xenograft tumor growth, while overexpression promoted aggressive phenotypes (p < 0.05). Mechanistically, ASNS was identified as a critical MACF1 target, with ATF4 serving as a transcriptional mediator linking MACF1 to ASNS regulation. Conclusion: Our findings demonstrate that MACF1 promotes CRC cell growth and migration, at least in part, via ATF4-associated ASNS regulation and asparagine metabolism. This work establishes a novel functional bridge between cytoskeletal remodeling and amino acid metabolic reprogramming in CRC, offering potential insights for future metabolism-oriented therapeutic strategies.

2026-08-17 | GSE343610 | GEO

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