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GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.
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GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.
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GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.
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GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.
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GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.
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GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.
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Image Search Results


GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.

Journal: International Journal of Biological Sciences

Article Title: LDHA Lactylation Drives Malignant Progression of Oral Squamous Cell Carcinoma via a Positive Feedback Loop with Lactate

doi: 10.7150/ijbs.136949

Figure Lengend Snippet: GCN5 plays role as the lactyltransferase of LDHA-K318 in OSCC. (A) Co-IP was performed to assess the association of LDHA with various lactyltransferases. Nala:10mM. (B) Colocalization of GCN5 and LDHA in cells. Magnification: ×60, Scale bar: 10μm. (C) The GCN5 inhibitor MB-3 (100uM) markedly decreased the LDHA-Kla levels. (D) Knockdown of GCN5 decreased LDHA-Kla levels. (E) IHC was employed to examine GCN5 expression in clinical OSCC specimens (Tomor=71, Adjacent=20). (F) Clinicopathological correlations between GCN5 and malignant progression in OSCC patients were analyzed. (G) GCN5 was highly expressed in OSCC cell lines. (H-J) Treatment with MB-3 (100μM) modulated the proliferative of LDHA-WT and LDHA-K318R cells (H-I), as well as the migratory and invasive capacity (J) Scale bar: 100μm. (K) Schematic of subcutaneous xenograft model establishment in NOD/SCID mice. (L-N) Effects of LDHA lactylation and GCN5 inhibitor MB-3 on OSCC subcutaneous xenografts. (O) HE and IHC staining for OSCC subcutaneous xenografts. Scale bar: 100μm, ns: not significant, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. All the data are presented as mean±SD from three independently performed experiments.

Article Snippet: Antibodies for western blotting : Pan Kla (1:1000, PTM-1401RM, PTM BIO, China, RRID: AB_2942013), LDHA (1:5000, 19987-1-AP, Proteintech, China), HA (1:5000, 51064-2-AP, Proteintech, China), CBP (1:1000, D6C5, CST, USA), P300 (1:1000, D8Z4E, CST, USA), GCN5 (1:1000, ER63516, HUABIO, China), AARS1 (1:10000, 87581-2-RR, Proteintech, China), PCAF (1:5000, 86917-1-RR, Proteintech, China), MOF (1:1000, 13842-1-AP, Proteintech, China), TIP60 (1:1000, 10827-1-AP, Proteintech, China), HDAC1 (1:10000 ,83624-1-RR, Proteintech, China), HDAC2 (1:10000, 67165-1-Ig, Proteintech, China), HDAC3 (1:10000, 81211-1-RR, Proteintech, China), HRP Conjugated GAPDH (1:100000, HA724237H, HUABIO, China), HRP Conjugated β-actin (1:50000, HA724235H, HUABIO, China), HRP Conjugated β-tubulin (1:10000, HA724236H, HUABIO, China), HRP Goat Anti-Rabbit IgG secondary antibody (1:4000, 7074, CST, USA) and HRP-conjugated Goat Anti-Mouse secondary antibody (1:4000, SA00001-1, Proteintech, China), IPKine HRP, Mouse Anti-Rabbit IgG LCS (1:2000, A25022, Abbkine, China).

Techniques: Co-Immunoprecipitation Assay, Knockdown, Expressing, Xenograft Assay, Immunohistochemistry