Journal: Cell Death & Disease

Article Title: PER1 suppresses glycolysis and cell proliferation in oral squamous cell carcinoma via the PER1/RACK1/PI3K signaling complex

doi: 10.1038/s41419-021-03563-5

Figure Lengend Snippet: A Western blot results showed that the expression levels of HK2, PKM2, and LDHA were significantly increased in RNAi-PER1-TSCCA cells and decreased in OE-PER1-SCC15 and OE-PER1-CAL27 cells. B – D The results of the glucose uptake, lactate production, and enzyme activity assays showed that glucose uptake, lactate production, and the enzymatic activity of HK, PK, and LDH were significantly increased in RNAi-PER1-TSCCA cells, while in OE-PER1-SCC15 and OE-PER1-CAL27 cells, glucose uptake, lactate production, and the enzymatic activity of HK, PK, and LDH were significantly decreased. E , F CCK-8 and MTT assays showed that the proliferation of RNAi-PER1-TSCCA cells was significantly increased, while that of OE-PER1-SCC15 and OE-PER1-CAL27 cells was significantly decreased. All data are from three independent experiments. The data are presented as the mean ± SD values ( n ≥ 3). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: To explore whether PER1 mediates the proliferation of OSCC cells through the glycolytic pathway, we added the HK2 inhibitor 2-DG (2-deoxy- d -glucose, HY-13966, MCE) to RNAi-PER1-TSCCA cells to inhibit glycolysis and then evaluated changes in cell proliferation.

Techniques: Western Blot, Expressing, Activity Assay, CCK-8 Assay

Journal: Cell Death & Disease

Article Title: PER1 suppresses glycolysis and cell proliferation in oral squamous cell carcinoma via the PER1/RACK1/PI3K signaling complex

doi: 10.1038/s41419-021-03563-5

Figure Lengend Snippet: A , B The results of RT-qPCR and western blotting showed that the mRNA and protein expression levels of PER1 were significantly decreased after knockdown of PER1 in OE-PER1-SCC15 cells. C Western blot results showed that the decrease in the expression of HK2, PKM2, and LDHA was significantly reversed after knockdown of PER1 in OE-PER1-SCC15 cells. D – F The glucose uptake, lactate production, and enzyme activity assay results showed that the decreases in glucose uptake, lactate production, and enzymatic activity of HK, PK, and LDH were significantly reversed after knockdown of PER1 in OE-PER1-SCC15 cells. G , H The CCK-8 assay and MTT assay showed that the decrease in proliferation was significantly reversed after knockdown of PER1 in OE-PER1-SCC15 cells. All data are from three independent experiments. The data are presented as the mean ± SD values ( n ≥ 3). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: To explore whether PER1 mediates the proliferation of OSCC cells through the glycolytic pathway, we added the HK2 inhibitor 2-DG (2-deoxy- d -glucose, HY-13966, MCE) to RNAi-PER1-TSCCA cells to inhibit glycolysis and then evaluated changes in cell proliferation.

Techniques: Quantitative RT-PCR, Western Blot, Expressing, Knockdown, Enzyme Activity Assay, Activity Assay, CCK-8 Assay, MTT Assay

Journal: Cell Death & Disease

Article Title: PER1 suppresses glycolysis and cell proliferation in oral squamous cell carcinoma via the PER1/RACK1/PI3K signaling complex

doi: 10.1038/s41419-021-03563-5

Figure Lengend Snippet: A Western blot results showed that the levels of PI3K and p-AKT in RNAi-PER1-TSCCA cells were significantly increased, while the levels of PI3K and p-AKT were significantly decreased in OE-PER1-SCC15 cells. B RT-qPCR results showed that there were no significant changes in the mRNA levels of PI3K and AKT in RNAi-PER1-TSCCA and OE-PER1-SCC15 cells. C Western blot results showed that the increases in the levels of p-AKT, HK2, PKM2, and LDHA were significantly reversed after artemisinin was added to RNAi-PER1-TSCCA cells. D – F After artemisinin addition, the increases in glucose uptake, lactate production, and the enzymatic activity of HK, PK, and LDH in RNAi-PER1-TSCCA cells were significantly reversed. G , H The CCK-8 assay and MTT assay showed that the increased proliferation of RNAi-PER1-TSCCA cells was significantly reversed after artemisinin addition. All data are from three independent experiments. The data are presented as the mean ± SD values ( n ≥ 3). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: To explore whether PER1 mediates the proliferation of OSCC cells through the glycolytic pathway, we added the HK2 inhibitor 2-DG (2-deoxy- d -glucose, HY-13966, MCE) to RNAi-PER1-TSCCA cells to inhibit glycolysis and then evaluated changes in cell proliferation.

Techniques: Western Blot, Quantitative RT-PCR, Activity Assay, CCK-8 Assay, MTT Assay

Journal: Cell Death & Disease

Article Title: PER1 suppresses glycolysis and cell proliferation in oral squamous cell carcinoma via the PER1/RACK1/PI3K signaling complex

doi: 10.1038/s41419-021-03563-5

Figure Lengend Snippet: A Western blot results showed that the increase in the expression of HK2, PKM2, and LDHA was significantly reversed after 2-DG was added to RNAi-PER1-TSCCA cells. B – D After 2-DG was added to RNAi-PER1-TSCCA cells, the increases in glucose uptake, lactate production, and the enzymatic activity of HK, PK, and LDH were significantly reversed. E , F The CCK-8 assay and MTT assay showed that the increased proliferation of RNAi-PER1-TSCCA cells was significantly reversed after 2-DG addition. All data are from three independent experiments. The data are presented as the mean ± SD values ( n ≥ 3). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: To explore whether PER1 mediates the proliferation of OSCC cells through the glycolytic pathway, we added the HK2 inhibitor 2-DG (2-deoxy- d -glucose, HY-13966, MCE) to RNAi-PER1-TSCCA cells to inhibit glycolysis and then evaluated changes in cell proliferation.

Techniques: Western Blot, Expressing, Activity Assay, CCK-8 Assay, MTT Assay

Journal: Cell Death & Disease

Article Title: PER1 suppresses glycolysis and cell proliferation in oral squamous cell carcinoma via the PER1/RACK1/PI3K signaling complex

doi: 10.1038/s41419-021-03563-5

Figure Lengend Snippet: A The curve of tumor growth in nude mice showed that the tumor formation rate in the OE-PER1-SCC15 group was significantly lower than that in the NC-SCC15 group. B The tumor weights and volumes in the OE-PER1-SCC15 group were significantly lower than those in the NC-SCC15 group. C Western blotting showed that the expression of PER1 in the OE-PER1-SCC15 group was significantly higher than that in the NC-SCC15 group, while the levels of PI3K, p-AKT, HK2, PKM2, LDHA, and Ki-67 in the OE-PER1-SCC15 group were significantly lower than those in the NC-SCC15 group. All data are from three independent experiments. The data are presented as the mean ± SD values ( n ≥ 3). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: To explore whether PER1 mediates the proliferation of OSCC cells through the glycolytic pathway, we added the HK2 inhibitor 2-DG (2-deoxy- d -glucose, HY-13966, MCE) to RNAi-PER1-TSCCA cells to inhibit glycolysis and then evaluated changes in cell proliferation.

Techniques: Western Blot, Expressing

Journal: Journal of Nanobiotechnology

Article Title: Biocompatible glyconanomaterials based on HPMA-copolymer for specific targeting of galectin-3

doi: 10.1186/s12951-018-0399-1

Figure Lengend Snippet: Competitive inhibition of Gal-3 binding to ASF by glycopolymers 24 – 39 determined by ELISA

Article Snippet: Lactose (Galβ1,4Glc) was bought from Lachema (CZ) and LacNAc (Galβ1,4GlcNAc) from Carbosynth Ltd. (UK). p -Nitrophenyl 2-acetamido-2-deoxy-β- d -galactopyranoside ( p NP-GalNAc) and p -nitrophenyl 2-acetamido-2-deoxy-β- d -glucopyranoside ( p NP-GlcNAc) were obtained from Gold Biotechnology (MO, USA).

Techniques: Inhibition, Binding Assay, Glycoproteomics