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CDKL3 promotes osteosarcoma progression by activating Akt/PKB

View ORCID ProfileAina He  Correspondence email, Lanjing Ma, Yujing Huang, Haijiao Zhang, Wei Duan, Zexu Li, View ORCID ProfileTeng Fei, Junqing Yuan, Hao Wu, Liguo Liu, Yueqing Bai, Wentao Dai, Yonggang Wang, Hongtao Li, Yong Sun, Yaling Wang, Chunyan Wang, Ting Yuan, Qingcheng Yang, Songhai Tian, Min Dong, View ORCID ProfileRen Sheng  Correspondence email, View ORCID ProfileDongxi Xiang  Correspondence email
Aina He
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
2Department of Urology, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA
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  • ORCID record for Aina He
  • For correspondence: anna_1188@126.com
Lanjing Ma
3College of Life and Health Sciences, Northeastern University, Shenyang, PR China
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Yujing Huang
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Haijiao Zhang
3College of Life and Health Sciences, Northeastern University, Shenyang, PR China
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Wei Duan
4School of Medicine and Centre for Molecular and Medical Research, Deakin University, Waurn Ponds, Victoria, Australia
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Zexu Li
3College of Life and Health Sciences, Northeastern University, Shenyang, PR China
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Teng Fei
3College of Life and Health Sciences, Northeastern University, Shenyang, PR China
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Junqing Yuan
5Department of Pathology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Hao Wu
6Department of Vascular Biology, Boston Children’s Hospital, Boston, MA, USA
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Liguo Liu
7Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Yueqing Bai
5Department of Pathology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Wentao Dai
8Shanghai Center for Bioinformation Technology and Shanghai Engineering Research Center of Pharmaceutical Translation, Shanghai Industrial Technology Institute, Shanghai, PR China
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Yonggang Wang
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Hongtao Li
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Yong Sun
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Yaling Wang
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Chunyan Wang
1Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Ting Yuan
9Department of Orthopedics, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Qingcheng Yang
9Department of Orthopedics, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, PR China
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Songhai Tian
2Department of Urology, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA
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Min Dong
2Department of Urology, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA
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Ren Sheng
3College of Life and Health Sciences, Northeastern University, Shenyang, PR China
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  • For correspondence: shengren1211@126.com
Dongxi Xiang
10Division of Genetics, Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA
11Department of Medicine, Harvard Medical School, Boston, MA, USA
12Shanghai Research Center of Biliary Tract Disease Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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  • ORCID record for Dongxi Xiang
  • For correspondence: dxiang@bwh.harvard.edu
Published 31 March 2020. DOI: 10.26508/lsa.202000648
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  • Figure 1.
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    Figure 1. Cyclin-dependent kinase–like 3 (CDKL3) promotes the growth of osteosarcoma (OS) cells.

    (A) Comparison of CDKL3 expression levels by qRT-PCR analysis between adjacent non-tumor tissues and OS tissues derived from four OS patients. Three OS and three non-OS tissues from each patient were collected and analyzed. Two housekeeping genes (ACTB and GAPDH) were included in this study to normalize the CDKL3 expression. (B) Cell growth analysis of U2OS cells transfected with indicated siRNAs. (C) Cell growth analysis of U2OS and Saos-2 cells with CDKL3-shRNA silencing (n = 5). (D) Colony formation assay of cells conducted in (C). Scale bar = 1 cm. (E) Representative colony images and quantitative analysis from (D) (n = 3). Scale bar = 200 μm. Error bars represent SD (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed t test.

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    Figure S1. CDKL family kinase expression levels in osteosarcoma (OS) patients.

    (A) Comparison of CDKL1, 2, 4, and 5 expression levels by qRT-PCR analysis between adjacent non-tumor and OS tissues. Relative mRNA levels were calculated using the 2−ΔCt method, with mean of ACTB and GAPDH as internal controls. CDKL3 expression in OS tissues was normalized to its paired non-tumor tissue from the same patient (n = 3). (B) CDKL family kinase expression in four OS patients (n = 3). Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed t test.

  • Figure S2.
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    Figure S2. Knockdown of cyclin-dependent kinase–like 3 (CDKL3) inhibited osteosarcoma (OS) cell growth.

    (A) qRT-PCR analysis in U2OS cells transfected with siRNAs. Error bars indicate SD (n = 3). (B) Western blotting confirming the knockdown of CDKL3 in U2OS cells. (C) qRT-PCR analysis in targeted cells transfected with shRNAs. Error bars indicate SD (n = 5). (D) Fluorescence photomicrographs of Saos-2 cells in consecutive 5 d after shCDKL3 infection at a magnification of 100×. Scale bar = 150 μm. (E) Fold change of cell count in consecutive 5 d, which equals to cell counts divided by the cell counts in the first day after infection. Control: Saos-2 cells infected with lentivirus containing control shRNA. shCDKL3: Saos-2 cells infected with lentivirus specific interfering of CDKL3 (n = 3). Error bars indicate SD (n = 3 or n = 5). ***P < 0.001, two-tailed t test.

    Source data are available for this figure.

    Source Data for Figure S2[LSA-2020-00648_SdataFS2B.ppt]

  • Figure 2.
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    Figure 2. Knockdown of cyclin-dependent kinase–like 3 (CDKL3) inhibited osteosarcoma (OS) cell invasion and migration.

    (A) Genomic DNA sequencing of CDKL3-KO clones. (B) CDKL3 expression in CDKL3-KO and parental cells by Western blot analysis. (C) Microscopy images of wound closure of parental, CDKL3-KO (U19), and CDKL3-rescued (Res) U2OS cells at 0, 24, and 48 h after scratching. Scale bar = 75 μm. (D) Quantification of the wounded area invaded during 48 h of U2OS cells (n = 3). (E) Quantification of wound healing speed (μm/h) of U2OS cells (n = 3). (F) Microscopy images of wound closure of parental, CDKL3-KO (S4), and CDKL3-rescued (Res) Saos-2 cells at 0, 24, and 48 h after scratching. Scale bar = 75 μm. (G) Quantification of the wounded area invaded during 48 h of Saos-2 cells (n = 3). (H) Quantification of wound healing speed (μm/h) of Saos-2 cells (n = 3). (I) Representative images of Transwell-invaded U2OS cells (purple stained, red arrows). Scale bar = 100 μm. (J) Quantification of stained/invaded cells in (I) (n = 3). (K) Representative images of Transwell-migrated U2OS cells (purple stained, red arrows). Scale bar = 100 μm. (L) Quantification of stained/migrated cells in (K) (n = 3). (M) Representative images of Transwell-invaded Saos-2 cells (purple stained, red arrows). Scale bar = 100 μm. (N) Quantification of stained/invaded cells in (M) (n = 3). (O) Representative images of Transwell-migrated Saos-2 cells (purple stained, red arrows). Scale bar = 100 μm. (P) Quantification of stained/migrated cells in (O) (n = 3). (Q) Representative images of senescent cells stained with CellEvent senescence green probe. Scale bar = 75 μm. (R) FACS analysis of green-stained senescent cells in (Q). (S) Quantification of senescent U2OS cells in (R) (n = 3). (T) Quantification of senescent Saos-2 cells (n = 3). Error bars indicate SD (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001. Statistical significance of the differences was estimated by unpaired two-tailed t test. Linear regression was run on the wound width data using the GraphPad Prism software.

    Source data are available for this figure.

    Source Data for Figure 2[LSA-2020-00648_SdataF2B.ppt]

  • Figure S3.
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    Figure S3. Generation of CDKL3-KO cells.

    (A) Schematic diagram showing the KO strategy of CDKL3. The sgRNA and PAM sequences were marked in purple and green, respectively. (B) Mapping of nucleic acid sequence and its corresponding amino acids on Sanger sequencing.

  • Figure S4.
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    Figure S4. Cyclin-dependent kinase–like 3 (CDKL3)-KO inhibits osteosarcoma (OS) cell growth.

    (A) Fold change of U2OS and Saos-2 cell growth at indicated time courses after cocultured with CDKL3-KO cells. (B) Representative images of FACS data from cell growth competition assay, U2OS, and Saos-2 cells (GFP+) were cocultured with CDKL3-KO U2OS and Saos-2 cells. Error bars represent SD (n = 4). *P < 0.05, ***P < 0.001, two-tailed t test.

  • Figure S5.
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    Figure S5. Morphology of migrating U2OS and Saos-2 cells derived from the wound healing assay.

    Migration cells (green arrows) show obvious tails lamellipodia (red circle). Scale bar = 75 μm.

  • Figure 3.
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    Figure 3. Knockdown of CDKL3 suppresses OS tumor growth in vivo.

    (A) Representative images of tumor xenografts obtained from the indicated groups. Scale bar = 1 cm. (B) Left: tumor volumes over treatment. Right: tumor weight at harvest. Error bars represent SD (n = 8). *P < 0.05, ***P < 0.001, two-tailed t test.

  • Figure 4.
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    Figure 4. Cyclin-dependent kinase–like 3 (CDKL3) inhibits autophagy in osteosarcoma (OS).

    (A) An outline of OS clinical dataset analysis (GEO accession: GSE21257). 33 out of 53 patient samples were selectively analyzed based on the CDKL3 expression level for the differential gene expression patterns. (B) Signaling pathway was mapped by the R package clusterProfiler. Upper and bottom figures represent down-regulated and up-regulated pathways (CDKL3 top 0.3 versus bottom 0.3), respectively. KEGG enrichment analysis using the clusterProfiler R package was performed on differential expressed genes with a strict cutoff of P < 0.01 and false discovery rate of less than 0.05. The size of the dot indicates the number of differentially expressed genes in the pathway. Color of the dot represents the value of Benjamini and Hochberg false discovery rate–adjusted P-value. (C) Molecular connection of PI3K-Akt and AMPK pathway in regulation of cell growth, autophagy, etc. This summarized mechanism was extracted from the GEO dataset GSE21257. mTORC1 plays key roles in eukaryotic cell metabolism by promoting cell growth and inhibiting autophagy and apoptosis. (D) Representative images of parental cells and CDKL3-KO U2OS and Saos-2 cells transfected with mRFP-eGFP-LC3, at normal conditions (DMEM with 10% FBS, control) or 6 h EBSS treatment (starvation). Colocalized mRFP and eGFP (yellow dots) indicate autophagosomes, only mRFP (red dots) indicates autolysosomes. Nuclei (blue) were labeled with DAPI. Scale bar = 5 μm. (E) Quantification of autophagosomes (eGFP+mRFP+; yellow) and autolysosomes (eGFP−mRFP+; red) per cell from (D) (n = 3). (F) Western blot analysis of LC3B, Beclin-1, and Atg5-Atg12 in indicated cells. The number below each blotting strip is intensity quantification derived from ImageJ. Error bars indicate SEM (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed t test.

    Source data are available for this figure.

    Source Data for Figure 4[LSA-2020-00648_SdataF4F.ppt]

  • Figure S6.
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    Figure S6. Apoptotic cell analysis of cyclin-dependent kinase–like 3 (CDKL3)-KO osteosarcoma (OS) cells.

    (A) FACS analysis of parental and CDKL3-KO U2OS and Saos-2 cell apoptosis. Magenta circle represents apoptotic cell population. Error bars represent SD (n = 3). (B) Caspase3 and Caspase8 immunoblotting to detect apoptosis status for parental and CDKL3-KO U2OS cell under normal or starvation conditions. Solid and hollowed triangles represent uncleaved and cleaved Caspase3 and Caspase8, respectively.

    Source data are available for this figure.

    Source Data for Figure S6[LSA-2020-00648_SdataFS6B.ppt]

  • Figure 5.
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    Figure 5. Cyclin-dependent kinase–like 3 (CDKL3) critically regulates Akt activation in osteosarcoma (OS).

    (A) Akt and mTOR activation under regular or starvation conditions in parental and CDKL3-KO U2OS cells. Upon CDKL3 KO, Akt and mTORC1 activation were significantly alleviated. The numbers below each blotting strip is intensity quantification by ImageJ. (B) The expression patterns of mTORC1 and FoxO downstream target genes confirm that CDKL3 regulates both pathways at the transcription level. Cells were cultured under the regular growth condition. (C) Overexpression of CDKL3 in U2OS cells causes hyper-activation of Akt in the presence and absence of FBS. (D) General working mechanism of rapamycin, AZD5363, and MK-2206. (E) U2OS cell growth under different conditions (n = 3). (F) Co-immunoprecipitation (Co-IP) reveals the physical interaction between HA-CDKL3 and Myc-Akt1. (G) Endogenous CDKL3 coexists with endogenous Akt shown by co-IP. (H) Schematic diagrams of Akt1 constructs for mapping. (I) Co-IP of HA-CDKL3 with different Akt1 constructs shows that the Akt kinase domain is indispensable for CDKL3 interaction. (I, J) Reverse IP of CDKL3 and Akt1 confirms the findings in (I). Error bars indicate SD (n = 3). *P < 0.05 parental DMSO versus CDKL3−/− DMSO, or parental rapamycin, or parental AZD5363, or parental MK-2206; **P < 0.01 CDKL3−/− DMSO versus CDKL3−/− rapamycin, or CDKL3−/− AZD5363, or CDKL3−/− MK-2206; ##P < 0.01 parental MK-2206 versus CDKL3−/− MK-2206. Statistical significance of the differences was estimated by unpaired two-tailed t test.

    Source data are available for this figure.

    Source Data for Figure 5[LSA-2020-00648_SdataF5A.ppt][LSA-2020-00648_SdataF5C.ppt][LSA-2020-00648_SdataF5F.ppt][LSA-2020-00648_SdataF5G.ppt][LSA-2020-00648_SdataF5I.ppt][LSA-2020-00648_SdataF5J.ppt]

  • Figure S7.
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    Figure S7. IC50 measurement of rapamycin, AZD5365, and MK-2206 in parental U2OS cells.

    Error bars represent SD (n = 4).

  • Figure S8.
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    Figure S8. HA-CDKL3 co-immunoprecipitates endogenous Akt.

    Source data are available for this figure.

    Source Data for Figure S8[LSA-2020-00648_SdataFS8.ppt]

  • Figure S9.
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    Figure S9. Protein mapping on cyclin-dependent kinase–like 3 (CDKL3).

    (A) Schematic drawing for CDKL FL (full-length), K (Kinase domain), ΔK (Truncation of kinase domain) constructs. (B) Co-immunoprecipitation of Myc-Akt and HA-CDKL3 revealed that the kinase domain of CDKL3 is responsible for Akt interaction.

    Source data are available for this figure.

    Source Data for Figure S9[LSA-2020-00648_SdataFS9B.ppt]

  • Figure S10.
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    Figure S10. Prediction of the structure interaction of human CDKL3 with the kinase domain of Akt1.

    (A) Ribbon representation of the predicted complex between human cyclin-dependent kinase–like 3 (CDKL3) (blue) and the kinase domain of Akt1 (green). Hydrogen bonds shown as the red broken lines. The crystal structures of human CDKL3 (PDB ID: 3ZDU) and Akt1 (PDB ID: 6BUU) were taken from PDB database. Akt1 was docked into the 3D structure of CDKL3 using ClusPro 2.0. Highest scoring model with good topologies is shown. Enlarged stick representation to the right highlights the interacting residues between CDKL3 and Akt1. (B) Interaction residues between CDKL3 and Akt1. Predicted interacting residues in CDKL3 and Akt1 and corresponding hydrogen (H) – bonds between the residues.

  • Figure 6.
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    Figure 6. Cyclin-dependent kinase–like 3 (CDKL3) defines poor prognosis and correlates with Akt phosphorylation in clinic.

    (A, B) Kaplan–Meier plots of overall survival (A) and metastasis-free survival (B) of 152 osteosarcoma (OS) patients, stratified by CDKL3 levels (− represents negative staining; +, ++, and +++ represent weak, intermediate, and strong staining, respectively). (C) Representative immunohistochemistry (IHC) images of OS biopsies with different levels of CDKL3 expression on an OS microarray containing 152 primary OS tissues samples. Scale bar = 500 μm. (D) Representative HE and IHC images of OS biopsies stained by CDKL3 and Ki67. Scale bar = 100 μm. (E) Quantitative analysis of Ki67 expression in OS patients with different levels of CDKL3 expression. (F) HE and IHC staining images of CDKL3, AKT, pAKT (p308), pAKT (ser473), and LC3 in representative CDKL3-positive and CDKL3-negative patients. Scale bar = 100 μm. (G) Western blot detection of CDKL3 and Akt phosphorylation in OS tissues and adjacent non-tumor tissues from three different patients. (H) Putative underlying mechanism that CDKL3 promotes OS progression. Overexpression of CDKL3 leads to increased phosphorylation of Akt, followed by governing mTORC1 and FoxO activities, likely independent of functions of PDK1, growth factors, or relevant receptors; this may inhibit autophagy and eventually promote OS development. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed t test.

    Source data are available for this figure.

    Source Data for Figure 6[LSA-2020-00648_SdataF6G.ppt]

Tables

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    Table 1.

    Patient characteristics.

    CharacteristicNumber (%)CDKL3 (−)CDKL3 (+)P-value
    Gender0.446
     Female61 (40.1)32 (43.2)29 (37.2)
     Male91 (59.9)42 (56.8)49 (62.8)
    Age/year0.888
     <1871 (46.7)35 (47.3)36 (46.2)
     ≥1881 (53.3)39 (52.7)42 (53.8)
    Tumor site1a
     Extremities148 (97.4)72 (97.3)76 (97.4)
     Non-extremities4 (2.6)2 (2.7)2 (2.6)
    Enneking’s surgical staging0.396
     I/II141 (92.8)70 (94.6)71 (91.0)
     III11 (7.2)4 (5.4)7 (9.0)
    Karnofsky performance status score0.726a
     ≥80146 (96.1)72 (97.3)74 (94.9)
     ≤706 (3.9)2 (2.7)4 (5.1)
    Neoadjuvant chemotherapy1b
     Yes150 (98.7)73 (98.6)77 (91.0)
     No2 (1.3)1 (1.4)1 (9.0)
    Pathological subtype0.242
     Conventional136 (89.5)64 (86.5)72 (92.3)
     Telangiectatic16 (10.5)10 (13.5)6 (7.7)
    Surgical0.173
     Amputation47 (30.9)19 (25.7)28 (35.9)
     Limb salvage105 (69.1)55 (74.3)50 (64.1)
    Local recurrence0.851
     Yes38 (25.0)18 (24.3)20 (25.6)
     No114 (75.0)56 (75.7)58 (74.4)
    Metastasis0.024
     Yes94 (61.8)39 (52.7)55 (70.5)
     No58 (38.2)35 (47.3)23 (29.5)
    • Pearson’s chi-squared test was used to compare clinical differences between patients with negative or positive of CDKL3.

    • ↵a Continuous correction chi-square test.

    • ↵b Fisher’s exact test.

Supplementary Materials

  • Figures
  • Tables
  • Table S1 Oligonucleotides information.

  • Table S2 CDKL3−/− cell lines information.

  • Table S3 Enrichment analysis of up- and down-regulated pathways derived from GEO data GSE21257.[LSA-2020-00648_TableS3_2.xlsx]

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CDKL3 promotes osteosarcoma via Akt/PKB
Aina He, Lanjing Ma, Yujing Huang, Haijiao Zhang, Wei Duan, Zexu Li, Teng Fei, Junqing Yuan, Hao Wu, Liguo Liu, Yueqing Bai, Wentao Dai, Yonggang Wang, Hongtao Li, Yong Sun, Yaling Wang, Chunyan Wang, Ting Yuan, Qingcheng Yang, Songhai Tian, Min Dong, Ren Sheng, Dongxi Xiang
Life Science Alliance Mar 2020, 3 (5) e202000648; DOI: 10.26508/lsa.202000648

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CDKL3 promotes osteosarcoma via Akt/PKB
Aina He, Lanjing Ma, Yujing Huang, Haijiao Zhang, Wei Duan, Zexu Li, Teng Fei, Junqing Yuan, Hao Wu, Liguo Liu, Yueqing Bai, Wentao Dai, Yonggang Wang, Hongtao Li, Yong Sun, Yaling Wang, Chunyan Wang, Ting Yuan, Qingcheng Yang, Songhai Tian, Min Dong, Ren Sheng, Dongxi Xiang
Life Science Alliance Mar 2020, 3 (5) e202000648; DOI: 10.26508/lsa.202000648
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Volume 3, No. 5
May 2020
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