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Cited by 36Multiple Myeloma Research and TreatmentsAdvanced Glycation End Products researchLymphoma Diagnosis and Treatment

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HMGB1 knockdown increases MM cell vulnerability by regulating autophagy and DNA damage repair

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Guo, Xing, He, Donghua, Zhang, Enfan, Chen, Jing, Chen, Qingxiao, Li, Yi, Yang, Li, Yang, Yang, Zhao, Yi, Wang, Gang, He, Jingsong, Cai, Zhen·2018·Journal of Experimental & Clinical Cancer Research
DOI 10.1186/s13046-018-0883-3PMC PMC6114506
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Abstract

BACKGROUND: With the development of novel therapeutic agents, the survival of multiple myeloma (MM) patients has much improved. However, the disease is incurable due to drug resistance. Previous studies have found that high-mobility group box 1 (HMGB1) is involved in inflammation, angiogenesis, DNA damage repair, and cancer invasion, progression, metastasis and drug resistance and that high HMGB1 expression is associated with poor MM prognosis, yet the role and mechanism of HMGB1 in MM remains unclear. METHODS: Through gene expression and Oncomine database analyses, we found that HMGB1 is associated with a poor prognosis in MM patients. RNA interference together with gene array analysis, cell proliferation and apoptosis assays, autophagy detection assays, western blotting, and in vivo xenograft models were employed to evaluate the effect of HMGB1 and the mechanism involved in MM drug resistance. RESULTS: MM cell lines and primary MM samples were found to express high levels of HMGB1, which was negatively associated with the 3-year survival of MM patients. HMGB1 knockdown in MM cells enhanced the inhibitory effect of chemotherapy with dexamethasone (Dex) via apoptosis induction. Furthermore, downregulation of HMGB1 activated the mTOR pathway, inhibited autophagy and increased DNA damage induced by Dex by modulating expression of related genes. In vivo, xenograft models showed that after Dex treatment, the tumor burden of HMGB1-knockdown mice was decreased compared with that of control mice. CONCLUSIONS: Our research shows that HMGB1 participates in autophagy and DNA damage repair and that downregulation of HMGB1 enhances the sensitivity of MM cells to Dex, suggesting that HMGB1 may serve as a target for MM treatment.

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Fig. 1 Expression of HMGB1 in MM cells. a, b: qRT-PCR (a) and western blotting (b) results of HMGB1 expression in MM cell lines; c: qRT-PCR results of HMGB1 expression in primary MM cells (cells from the bone marrow of MM patients sorted by CD138 antibody beads); d: Expression of HMGB1 in the bone marrow tissue of MM patients, as evaluated by immunofluorescence; e: HMGB1 expression was negatively associated with MM patient 3-year survival according to the analysis of the Oncomine database (*p < 0.05)
Fig. 1 Expression of HMGB1 in MM cells. a, b: qRT-PCR (a) and western blotting (b) results of HMGB1 expression in MM cell lines; c: qRT-PCR results of HMGB1 expression in primary MM cells (cells from the bone marrow of MM patients sorted by CD138 antibody beads); d: Expression of HMGB1 in the bone marrow tissue of MM patients, as evaluated by immunofluorescence; e: HMGB1 expression was negatively associated with MM patient 3-year survival according to the analysis of the Oncomine database (*p < 0.05)CC BY · PubMed Central
Fig. 2 HMGB1 knockdown enhanced the inhibitory effect of chemotherapy in MM cells. a: MM cells (RPMI8226, CAG, MM.1S) were transfected with HMGB1 knockdown lentivirus, and the transfection effect was observed with a fluorescence microscope; b, c, d: qRT-PCR (b), western blot and densitometric analysis of the western blot results (c) were used to verify HMGB1 knockdown effect (n = 3); d: The CCK8 assay was used to determine the proliferation of MM cells after HMGB1 knockdown (n = 3, p > 0.05); e: The CCK8 assay was used to analyze the inhibitory effect of Dex after HMGB1 knockdown (n = 3, P>0.05) (*P<0.05,**P<0.01,***P<0.001)
Fig. 2 HMGB1 knockdown enhanced the inhibitory effect of chemotherapy in MM cells. a: MM cells (RPMI8226, CAG, MM.1S) were transfected with HMGB1 knockdown lentivirus, and the transfection effect was observed with a fluorescence microscope; b, c, d: qRT-PCR (b), western blot and densitometric analysis of the western blot results (c) were used to verify HMGB1 knockdown effect (n = 3); d: The CCK8 assay was used to determine the proliferation of MM cells after HMGB1 knockdown (n = 3, p > 0.05); e: The CCK8 assay was used to analyze the inhibitory effect of Dex after HMGB1 knockdown (n = 3, P>0.05) (*P<0.05,**P<0.01,***P<0.001)CC BY · PubMed Central
Fig. 3 HMGB1 knockdown increased Dex-induced MM cell apoptosis. a: RPMI8226 and CAG were treated with Dex for 48 h, and cell cycle distribution was detected by flow cytometry (n = 3, p > 0.05); b: Representative flow cytometry results showing RPMI 82286 (transfected with control shRNA or HMGB1 shRNA) apoptosis after treatment with Dex (100 μM) for 48 h; c: Histograms showing the results of the analysis of cell apoptosis induced by Dex (n = 3); d: Western blotting was performed to detect the expression of c-caspase-3 and c-PARP induced by Dex after HMGB1 knockdown; e: Histograms showing the densitometric analysis of the 15 KD fragment of c-caspase-3 (*P<0.05,**P<0.01,***P<0.001)
Fig. 3 HMGB1 knockdown increased Dex-induced MM cell apoptosis. a: RPMI8226 and CAG were treated with Dex for 48 h, and cell cycle distribution was detected by flow cytometry (n = 3, p > 0.05); b: Representative flow cytometry results showing RPMI 82286 (transfected with control shRNA or HMGB1 shRNA) apoptosis after treatment with Dex (100 μM) for 48 h; c: Histograms showing the results of the analysis of cell apoptosis induced by Dex (n = 3); d: Western blotting was performed to detect the expression of c-caspase-3 and c-PARP induced by Dex after HMGB1 knockdown; e: Histograms showing the densitometric analysis of the 15 KD fragment of c-caspase-3 (*P<0.05,**P<0.01,***P<0.001)CC BY · PubMed Central
Fig. 4 Changes of MM survival and apoptosis related genes after HMGB1 knockdown. a: Heatmap of the Affymetrix HTA 2.0 array results in RPMI8226 and CAG cells showing that the DEPTOR, Bcl-2, Bcl-xl, and Mcl1 levels were decreased; b, c,: qRT-PCR (B) and western blotting (c) were used to verify the array results; d: Densitometric analysis of the protein levels of DEPTOR, Bcl-2, and Bcl-xl (n = 3, *p < 0.05, **p < 0.01, ***p < 0.001)
Fig. 4 Changes of MM survival and apoptosis related genes after HMGB1 knockdown. a: Heatmap of the Affymetrix HTA 2.0 array results in RPMI8226 and CAG cells showing that the DEPTOR, Bcl-2, Bcl-xl, and Mcl1 levels were decreased; b, c,: qRT-PCR (B) and western blotting (c) were used to verify the array results; d: Densitometric analysis of the protein levels of DEPTOR, Bcl-2, and Bcl-xl (n = 3, *p < 0.05, **p < 0.01, ***p < 0.001)CC BY · PubMed Central
Fig. 5 mTOR pathway was activated, autophagy was inhibited after HMGB1 knockdown and the enhanced sensitivity effect of HMGB1 knockdown was blocked by CQ (an autophagy inhibitor). a: Western blotting was performed to analyze changes in the mTOR pathway after HMGB1 knockdown; the phosphorylation of p70S6K (substrate of the mTORC1 complex) and AKT-ser473 (substrate of the mTORC2 complex) were both increased; b: Densitometric analysis of the phosphorylation of mTOR, p70S6K and AKT; c: Representative results showing the fluorescence intensities in RPMI8226 after Dex (100 μM) exposure using the Cyto-ID Autophagy Detection Kit with flow cytometry, control shRNA without Dex (red line), HMGB1 shRNA without Dex (blue line), control shRNA with Dex (orange line), and HMGB1 shRNA with Dex (green line); d: Histograms showing the analysis results of the MM cell lines(RPMI8226, CAG) autophagy fluorescence intensities induced by Dex after HMGB1 knockdow by Cyto-ID Autophagy Detection Kit n (n = 3); e: Western blotting was performed to detect the Dex-induced expression of LC3A/B-I/II after HMGB1 knockdown and the histograms showing the densitometric analysis of LC3A/B-II; f: Histograms showing the analysis results of RPMI8226 (transfection with control shRNA or HMGB1 shRNA) apoptosis induced by Dex (100 μM) in the presence of CQ (1 μM, an autophagy inhibitor) (*P<0.05,**P<0.01,***P<0.001)
Fig. 5 mTOR pathway was activated, autophagy was inhibited after HMGB1 knockdown and the enhanced sensitivity effect of HMGB1 knockdown was blocked by CQ (an autophagy inhibitor). a: Western blotting was performed to analyze changes in the mTOR pathway after HMGB1 knockdown; the phosphorylation of p70S6K (substrate of the mTORC1 complex) and AKT-ser473 (substrate of the mTORC2 complex) were both increased; b: Densitometric analysis of the phosphorylation of mTOR, p70S6K and AKT; c: Representative results showing the fluorescence intensities in RPMI8226 after Dex (100 μM) exposure using the Cyto-ID Autophagy Detection Kit with flow cytometry, control shRNA without Dex (red line), HMGB1 shRNA without Dex (blue line), control shRNA with Dex (orange line), and HMGB1 shRNA with Dex (green line); d: Histograms showing the analysis results of the MM cell lines(RPMI8226, CAG) autophagy fluorescence intensities induced by Dex after HMGB1 knockdow by Cyto-ID Autophagy Detection Kit n (n = 3); e: Western blotting was performed to detect the Dex-induced expression of LC3A/B-I/II after HMGB1 knockdown and the histograms showing the densitometric analysis of LC3A/B-II; f: Histograms showing the analysis results of RPMI8226 (transfection with control shRNA or HMGB1 shRNA) apoptosis induced by Dex (100 μM) in the presence of CQ (1 μM, an autophagy inhibitor) (*P<0.05,**P<0.01,***P<0.001)CC BY · PubMed Central
Fig. 6 DNA damage induced by Dex was increased after HMGB1 knockdown. a, c: Western blotting was performed to evaluate the expression of the DNA damage and repair related proteins Rad51 (a) and γH2A.X (c), respectively, after HMGB1 knockdown with or without Dex exposure for 48 h; b, d:Densitometric analysis of Rad51 (b) and γH2A.X (d); e: Histograms showing the analysis results of RPMI8226 (transfection with control shRNA or HMGB1 shRNA) apoptosis induced by Dex (100 μM) in presence of AZD6738 (2 μM, an ATR inhibitor) (*P<0.05,**P<0.01,***P<0.001)
Fig. 6 DNA damage induced by Dex was increased after HMGB1 knockdown. a, c: Western blotting was performed to evaluate the expression of the DNA damage and repair related proteins Rad51 (a) and γH2A.X (c), respectively, after HMGB1 knockdown with or without Dex exposure for 48 h; b, d:Densitometric analysis of Rad51 (b) and γH2A.X (d); e: Histograms showing the analysis results of RPMI8226 (transfection with control shRNA or HMGB1 shRNA) apoptosis induced by Dex (100 μM) in presence of AZD6738 (2 μM, an ATR inhibitor) (*P<0.05,**P<0.01,***P<0.001)CC BY · PubMed Central
Fig. 7 HMGB1 knockdown increased the sensitivity of MM cells to Dex in vivo. a, b: Tumor volume, as measured by Vernier calipers in the four different groups (six mice per group). c, d: Immunohistochemical analysis was performed to detect the expression of HMGB1, DEPTOR, Bcl-2, c-caspase-3,γH2A.X, Rad51 and pAKt(ser473)(magnification: 400×) (*P<0.05)
Fig. 7 HMGB1 knockdown increased the sensitivity of MM cells to Dex in vivo. a, b: Tumor volume, as measured by Vernier calipers in the four different groups (six mice per group). c, d: Immunohistochemical analysis was performed to detect the expression of HMGB1, DEPTOR, Bcl-2, c-caspase-3,γH2A.X, Rad51 and pAKt(ser473)(magnification: 400×) (*P<0.05)CC BY · PubMed Central

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Metadata

Authors
Guo, X., He, D., Zhang, E., Chen, J., Chen, Q., Li, Y., Yang, L., Yang, Y., Zhao, Y., Wang, G., He, J., & Cai, Z.
Affiliations
  • First Affiliated Hospital Zhejiang University (CN)
  • Quzhou City People's Hospital (CN)
Corresponding author
Cai, Zhen
ORCID
Venue
Journal of Experimental & Clinical Cancer Research
Publisher
Springer Science and Business Media LLC
Published
2018-08-29
Volume
37
Issue
1
Pages
205-205
ISSN
  • 0392-9078 (ISSN-L)
  • 1756-9966
DOI
10.1186/s13046-018-0883-3
PMC
PMC6114506
OpenAlex
W2888919844
Cited by
36
References
2
Citations by year
2025: 6 · 2024: 3 · 2023: 9 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 5
FWCI
2.51
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Experimental & Clinical Cancer Research (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (81201868, 81471532, 31311380)
  • Specialized Research Fund for the Doctoral Program of Higher Education (20120101120100)
  • Zhejiang Provincial Natural Science Foundation of China (LY16H080001)
Topics
  • Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
Keywords
HMGB1, multiple myeloma, autophagy, DNA repair, dexamethasone, drug resistance, mTOR signaling, apoptosis, prognosis, therapeutic target
MeSH terms
Animals, Autophagy, Dexamethasone, DNA Damage, DNA Repair, Humans, Multiple Myeloma, Gene Expression Regulation, Neoplastic, Apoptosis, Drug Resistance, Neoplasm, Xenograft Model Antitumor Assays, HMGB1 Protein, RNA, Small Interfering, Cell Line, Tumor, Cell Proliferation, Mice

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