Static Magnetic Field (0.2-0.4 T) Stimulates the Self-Renewal Ability of Osteosarcoma Stem Cells Through Autophagic Degradation of Ferritin
← Research streamProlonged exposure to a moderate-intensity static magnetic field (0.2–0.4 T) increased proliferation and tumorsphere formation in K7M2 and MG63 osteosarcoma stem cells and was associated with increased Fe2+ release, ROS, and markers consistent with ferritinop…
Study snapshot
Abstract
Static Magnetic Field (0.2-0.4 T) Stimulates the Self-Renewal Ability of Osteosarcoma Stem Cells Through Autophagic Degradation of Ferritin Bin Zhao, Tongyao Yu, Shenghang Wang, Jingmin Che, Liangfu Zhou, Peng Shang. Static Magnetic Field (0.2-0.4 T) Stimulates the Self-Renewal Ability of Osteosarcoma Stem Cells Through Autophagic Degradation of Ferritin. Bioelectromagnetics. 2021 Jun 3. doi: 10.1002/bem.22352. Abstract Static magnetic field (SMF) can alter cell fate decisions in many ways. However, the effects of SMF on cancer stem cells (CSCs) are little-known. In this particular study, we evaluate the biological effect of moderate- intensity SMF on osteosarcoma stem cells (OSCs) and try to clarify the underlying mechanisms of action. First, we demonstrated that prolonged exposure to SMF induced the proliferation and tumorsphere formation in K7M2 and MG63 OSCs. Moreover, SMF promoted the release of ferrous iron (Fe2+ ) and provoked reactive oxygen species (ROS) in OSCs. Interestingly, SMF evidently triggered the autophagic degradation of ferritin, which is characterized by the activation of microtubule-associated protein 1 light chain 3 (LC3) and nuclear receptor co-activator 4 (NCOA4), and downregulation of ferritin heavy chain 1 (FTH1) in OSCs. Particularly, the colony-forming ability of K7M2 OSCs promoted by SMF was obviously abolished by using a small interfering RNA (siRNA) against NCOA4. Finally, treatment of the tumor-bearing mice with SMF did not affect the tumor volume or tumor mass, nor pulmonary metastasis of K7M2 OSCs, but the SMF-treated K7M2 OSCs caused a preference of pulmonary metastasis in a mouse model, which suggested that SMF might induce the metastatic characteristic of OSCs. Consequently, this paper demonstrates for the first time that the cumulative SMF exposure promoted the self-renewal ability of OSCs via autophagic degradation of ferritin, implying that ferritinophagy may be a potential molecular target for cancer. pubmed.ncbi.nlm.nih.gov Conclusions Our study has provided, to our knowledge, the first evidence that moderate-intensity SMF stimulated the self- renewal ability of OSCs through autophagic degradation of ferritin (Fig. 7a). The long-term exposure to moderate-intensity SMF did not affect the tumor volume or tumor mass, nor the lung metastasis in tumor- bearing mice, but the OSCs exposed to SMF did cause a preference of pulmonary metastasis in tumor-bearing mice (Fig. 7b). Finally, it is important to state that the effects of SMF on OSCs here are not directly applicable to humans and should be interpreted with caution.
AI evidence extraction
Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.
Main findings
Prolonged exposure to a moderate-intensity static magnetic field (0.2–0.4 T) increased proliferation and tumorsphere formation in K7M2 and MG63 osteosarcoma stem cells and was associated with increased Fe2+ release, ROS, and markers consistent with ferritinophagy (LC3 and NCOA4 activation; FTH1 downregulation). In tumor-bearing mice, SMF treatment did not change tumor volume/mass or pulmonary metastasis, but SMF-exposed K7M2 cells showed a preference of pulmonary metastasis in a mouse model; the SMF-enhanced colony-forming ability was abolished by NCOA4 siRNA.
Outcomes measured
- Cell proliferation
- Tumorsphere formation
- Ferrous iron (Fe2+) release
- Reactive oxygen species (ROS)
- Autophagic degradation of ferritin (LC3, NCOA4 activation; FTH1 downregulation)
- Colony-forming ability (with NCOA4 siRNA intervention)
- Tumor volume
- Tumor mass
- Pulmonary metastasis / preference of pulmonary metastasis
Limitations
- Exposure duration details not specified in the abstract
- Sample sizes not reported in the abstract
- Authors note effects on osteosarcoma stem cells are not directly applicable to humans and should be interpreted with caution
View raw extracted JSON
{
"study_type": "animal",
"exposure": {
"band": "static",
"source": null,
"frequency_mhz": null,
"sar_wkg": null,
"duration": "prolonged/long-term exposure (not further specified)"
},
"population": "Osteosarcoma stem cells (K7M2 and MG63) and tumor-bearing mice (K7M2 model)",
"sample_size": null,
"outcomes": [
"Cell proliferation",
"Tumorsphere formation",
"Ferrous iron (Fe2+) release",
"Reactive oxygen species (ROS)",
"Autophagic degradation of ferritin (LC3, NCOA4 activation; FTH1 downregulation)",
"Colony-forming ability (with NCOA4 siRNA intervention)",
"Tumor volume",
"Tumor mass",
"Pulmonary metastasis / preference of pulmonary metastasis"
],
"main_findings": "Prolonged exposure to a moderate-intensity static magnetic field (0.2–0.4 T) increased proliferation and tumorsphere formation in K7M2 and MG63 osteosarcoma stem cells and was associated with increased Fe2+ release, ROS, and markers consistent with ferritinophagy (LC3 and NCOA4 activation; FTH1 downregulation). In tumor-bearing mice, SMF treatment did not change tumor volume/mass or pulmonary metastasis, but SMF-exposed K7M2 cells showed a preference of pulmonary metastasis in a mouse model; the SMF-enhanced colony-forming ability was abolished by NCOA4 siRNA.",
"effect_direction": "mixed",
"limitations": [
"Exposure duration details not specified in the abstract",
"Sample sizes not reported in the abstract",
"Authors note effects on osteosarcoma stem cells are not directly applicable to humans and should be interpreted with caution"
],
"evidence_strength": "low",
"confidence": 0.74,
"peer_reviewed_likely": "yes",
"keywords": [
"static magnetic field",
"SMF",
"0.2-0.4 T",
"osteosarcoma stem cells",
"cancer stem cells",
"self-renewal",
"proliferation",
"tumorsphere",
"ferritinophagy",
"autophagy",
"NCOA4",
"LC3",
"FTH1",
"ROS",
"Fe2+",
"mouse model",
"pulmonary metastasis"
],
"suggested_hubs": []
}AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.
Identifiers and source
DOI: 10.1002/bem.22352
PubMed: 34082485
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