Objective:To investigate the role and molecular mechanisms of transcription factor EB (TFEB) and its target genes in the treatment of multiple myeloma (MM) with bortezomib.Methods:TFEB target genes were predicted using the GTRD database (http://gtrd.biouml.org/), identifying Ptch1 gene for further study. Expression changes of Ptch1 in RPMI8226 and U266 MM cell lines after bortezomib treatment were assessed by real time fluorogenic quantitative PCR (RT-qPCR) and Western blot. RPMI8226 and U266 cell lines were transfected with siRNA-TFEB, and mRNA and protein levels of key factors (Ptch1, Gli1) in the Ptch1/Hedgehog signaling pathway were measured by RT-qPCR and Western blot. Furthermore, Ptch1 was overexpressed in MM cell lines via lentiviral transduction. Autophagy was evaluated by acridine orange staining, and protein levels of LC3B, Beclin-1, and Lamp-1 were measured by Western blot. Lysosomal quantity changes were assessed by lysosomal fluorescent probes.Results:Bortezomib (6.0×10 -6 mmol/L, 24 h) significantly reduced Ptch1 mRNA and protein levels in both cell lines compared with blank control group (all P<0.05). siRNA-TFEB transfection reversed bortezomib’s inhibition of Hedgehog pathway key factors Ptch1 and Gli. Ptch1 overexpression in bortezomib-treated RPMI8226 and U266 cells significantly reduced the relative expression of autophagy-related proteins LC3B, Beclin-1, and Lamp-1 (all P=0.001). Acridine orange staining showed fewer acidic vesicular organelles within two cell lines (all P=0.001). The relative fluorescence expressions of lysosomal probes reflecting the number of lysosomes were also decreased ( P values of RPMI8226 and U266 cell lines were 0.001 and 0.007, respectively) . Conclusion:The knockdown of TFEB can specifically promote the expression of the Ptch1/Hedgehog signaling pathway, thereby reducing bortezomib-induced autophagy in MM cells and reversing the inhibitory effect of bortezomib on the proliferation of MM cell lines.

Objective:To investigate the role and molecular mechanisms of transcription factor EB (TFEB) and its target genes in the treatment of multiple myeloma (MM) with bortezomib.Methods:TFEB target genes were predicted using the GTRD database (http://gtrd.biouml.org/), identifying Ptch1 gene for further study. Expression changes of Ptch1 in RPMI8226 and U266 MM cell lines after bortezomib treatment were assessed by real time fluorogenic quantitative PCR (RT-qPCR) and Western blot. RPMI8226 and U266 cell lines were transfected with siRNA-TFEB, and mRNA and protein levels of key factors (Ptch1, Gli1) in the Ptch1/Hedgehog signaling pathway were measured by RT-qPCR and Western blot. Furthermore, Ptch1 was overexpressed in MM cell lines via lentiviral transduction. Autophagy was evaluated by acridine orange staining, and protein levels of LC3B, Beclin-1, and Lamp-1 were measured by Western blot. Lysosomal quantity changes were assessed by lysosomal fluorescent probes.Results:Bortezomib (6.0×10 -6 mmol/L, 24 h) significantly reduced Ptch1 mRNA and protein levels in both cell lines compared with blank control group (all P<0.05). siRNA-TFEB transfection reversed bortezomib’s inhibition of Hedgehog pathway key factors Ptch1 and Gli. Ptch1 overexpression in bortezomib-treated RPMI8226 and U266 cells significantly reduced the relative expression of autophagy-related proteins LC3B, Beclin-1, and Lamp-1 (all P=0.001). Acridine orange staining showed fewer acidic vesicular organelles within two cell lines (all P=0.001). The relative fluorescence expressions of lysosomal probes reflecting the number of lysosomes were also decreased ( P values of RPMI8226 and U266 cell lines were 0.001 and 0.007, respectively) . Conclusion:The knockdown of TFEB can specifically promote the expression of the Ptch1/Hedgehog signaling pathway, thereby reducing bortezomib-induced autophagy in MM cells and reversing the inhibitory effect of bortezomib on the proliferation of MM cell lines.

Objective:To construct a follow-up evaluation index system for "Diagnosis of Brucellosis" (WS 269-2019), and provide a reference basis for the next revision and improvement of the standard.Methods:The evaluation index system for "Diagnosis of Brucellosis" (WS 269-2019) was preliminarily established by consulting relevant references and materials. The experts in the field of diagnosis, treatment, prevention and control of brucellosis were selected, and two rounds of expert consultation were carried out in the form of questionnaires using the Delphi method. The necessity and availability of evaluation indicators were scored, and suggestions for modifying and adding indicators were put forward. Based on this, a standard follow-up evaluation index system was established. At the same time, a judgment matrix was constructed combined with the Saaty scale, and the analytic hierarchy process was used to calculate the weight of each index in the system.Results:After 2 rounds of expert ( n = 10) consultation, a standard follow-up evaluation index system for "Diagnosis of Brucellosis" (WS 269-2019) was constructed with 3 first-level indexes, 8 second-level indexes and 21 third-level indexes. The positive coefficients of experts in 2 rounds of questionnaires were both 100%; the coefficient of authority of experts was 0.82; the Kendall's coefficients of concordance of first-level, second-level and third-level indexes were 0.722, 0.260, and 0.181, respectively, with P < 0.05. Among the first-level indexes, the weight of standard quality evaluation was the highest (0.364), and the weight of standard implementation status was the lowest (0.278); among the second-level indexes, the combined weight of social benefits was the highest (0.186), and the combined weight of advanced nature was the lowest (0.043); among the third-level indexes, the combined weight of timely diagnosis rate was the highest (0.096), and the combined weight of consistency with technical data was the lowest (0.009). Conclusions:The constructed follow-up evaluation index system for "Diagnosis of Brucellosis" (WS 269-2019) is scientific and reliable, which evaluated qualitatively and quantitatively, reduces the defects of a single evaluation, and provides a basis for subsequent revision and improvement of the standard.

Based on the main problems existing in the current way of handling medical disputes, the authors explored a new method for handling medical disputes, and summarized the advantages of the mode of mediation studio specially invited by the people′s court. This mode effectively connected the traditional medical dispute resolution approaches, complemented each other′s advantages, and provided a faster, more efficient and national compulsory solution for medical disputes.

Objective:To investigate the effect of GTPBP4 silencing by RNA interference on the radiosensitivity of esphageal cancer EC9706 cells line.Methods:The expression data of GTPBP4 in esophageal cancer tissues was obtained from public Gene Expression Omnibus (GEO) database. Recombinant plasmid-mediated RNA interference (RNAi) was employed to transfect the esophageal cancer EC9706 cell to evaluate the influence of GTPBP4 silencing on the proliferation, apoptosis and radiosensitivity of esphageal cancer EC9706 cells. The expression levels of GTPBP4 mRNA and protein and apoptosis-associated proteins of Bax, cleaved caspase-9, cleaved caspase-3 and Bcl-2 were determined by qRT-PCR and Western blot. The cell proliferation was determined by MTT assay. The changes in cell apoptosis were detected AnnexinⅤ-FITC/PI double staining flow cytometry. The variations in radiosensitivity after radiation exposure were assessed by clone formation assay.Results:The expression level of GTPBP4 in the esophageal cancer tissues was significantly higher than that in the normal adjacent esophageal tissues ( P<0.001). qRT-PCR and Western blot demonstrated that the expression levels of GTPBP4 mRNA and protein in the GTPBP4-siRNA group were significantly lower than those in the blank and negative control groups (both P<0.001), suggesting that the plasmid was successfully transfected into the EC9706 cells. MTT assay indicated that the EC9706 cell proliferation rate was significantly inhibited ( P<0.001). Flow cytometry found that the apoptosis rate was significantly increased in the GTPBP4-siRNA group ( P<0.001). After GTPBP4 gene interference combined with radiotherapy, the cell sensitivity enhancement ratio was 1.716. The apoptosis rate of EC9706 cells was significantly increased in the GTPBP4-siRNA group ( P<0.001). The expression levels of apoptosis-associated proteins including cleaved caspase-9, cleaved caspase-3 and Bax were significantly up-regulated, whereas that of Bcl-2 was significantly down-regulated in the EC9706 cells in the GTPBP4-siRNA group ( P<0.001, P=0.001, P=0.001 and P=0.005). Conclusions:GTPBP4 gene is highly expressed in human esophageal cancer tissues. RNAi technology can effectively inhibit the expression of GTPBP4 gene in the EC9706 cells, thereby suppressing cell proliferation, inducing cell apoptosis and enhancing the radiosensitivity of cells.

Objective: To investigate the effects of c-Met inhibitor AMG-102 on the proliferation and apoptosis of laryngeal squamous carcinoma Hep-2 cells and the underlying mechanism. Methods: Laryngeal squamous carcinoma cell line Hep-2 cells were treated with 2.5, 5 and 10 μmol/L AMG-102, respectively. The proliferation activities of Hep-2 cells were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT). The apoptotic rate of Hep-2 cells was detected by flow cytometry analysis and Hoechst staining. The mRNA expression levels of apoptosis-related genes were detected by real-time quantitative polymerase Chain reaction (RT-qPCR), and the protein expressions of c-Met/PI3K/AKT pathway were detected by western blot. Results: Compared with the control group, the proliferation rates of Hep-2 cells treated with 2.5, 5 and 10 μmol/L AMG-102 for 24 hours were (89.8±1.1)%, (79.8±1.0)% and (69.1±1.2)%, respectively; for 48 hours were (76.8±2.0)%, (60.2±1.1)% and (49.8±1.2)%, respectively; for 72 hours were (50.1±2.0)%, (41.5±1.1)% and (33.6±1.0), respectively, with significant differences (all P<0.05). The apoptotic rates of Hep-2 cells treated with 2.5, 5 and 10 μmol/L AMG-102 for 48 hours were (16.09±1.53)%, (27.51±2.02)% and (36.57±1.42)%, respectively, which were significantly higher than (3.62±0.10) % in the control group (all P<0.05). After treated with 2.5, 5 and 10 μmol/L AMG-102 for 48 hours, the relative expression levels of Bcl-2 mRNA in Hep-2 cells were 0.58±0.13, 0.38±0.12 and 0.20±0.13, respectively; the relative protein expression of p-Met were 80.0±3.8, 50.6±4.2 and 28.5±1.3, respectively; the relative protein expression of p-PI3K were 87.1±0.9, 54.2±1.2 and 21.0±1.2, respectively; the relative protein expression of p-AKT were 98.7±5.6, 56.9±3.2 and 32.2±4.3, respectively; which were significantly lower than those in the control group (all P<0.05). The relative expression levels of Bax mRNA were 1.78±0.13, 2.37±0.14 and 3.05±0.13, respectively, and the relative expression levels of caspase-3 mRNA were 1.98±0.14, 2.47±0.14 and 3.15±0.13, respectively, which were significantly higher than those in the control group (all P<0.05). Conclusion c-Met inhibitor AMG-102 could inhibit the proliferation and induce apoptosis of laryngeal squamous carcinoma Hep-2 cells by regulating the c-Met/PI3K/Akt pathway.

Objective　To investigate the prognostic value of NLR,PLR,PNR and PWR in acute cerebral infarction.Methods　We enrolled 139 patients who were diagnosed with acute cerebral infarction from Chengde Central Hospital from September 2018 to September 2019.Routine blood test results were collected.Patients were divided into mild stroke and moderate-severe stroke groups according to the NIHSS at admission.After three months,subjects were divided into two groups according to the modified Rankin score (mRS),one group with good prognosis (mRS 0~2) and the other with poor prognosis (mRS 3~6).Logistic regression analysis was performed,the ROC curve was used to evaluate inflammatory markers in predicting prognosis.Results　After adjusting for confounders,PLR and NLR in the group with good prognosis were significantly lower than that of the other group (P<0.005),PWR was higher in good prognosis group (P<0.05).In addition,PLR and NLR in the mild stroke group were significantly lower than the moderate-severe stoke group (P<0.05).The ROC curve showed that the area under the curve of PLR and NLR for predicting the prognosis of acute cerebral infarction at 3 months was 0.721 (95%CI 0.630~0.813;P<0.001),0.765 (95%CI 0.678~0.851;P<0.001) and the area under the curve of the PWR is 0.642.Conclusion　NLR and PLR,as new inflammatory indicators,may be independent factors for predicting the prognosis of AIS,and can also be used to judge the severity of stroke.

Objective: To investigate the effect of c-Met inhibitor AMG-102 on proliferation and radiosensitivity in laryngeal squamous carcinoma cells. Methods: The effects of AMG-102 on proliferation and radiosensitivity of laryngeal squamous carcinoma cell lines Hep-2 and KBV200 were detected by 3-(4, 5-dimethy-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay and colony formation assay, respectively. The apoptosis of Hep-2 and KBV200 cells was detected by flow cytometry. The expression levels of c-Met, phospho-Met (p-Met), cleaved caspase-3 and Akt/p-Akt, Erk/p-Erk were detected by Western blot. Specific small interfering RNA targeting c-Met or plasmid of c-Met were transfected into Hep-2 and KBV200 cells to investigate the cell sensitivity to AMG-102. Results: Compared with KBV200 cells, Hep-2 cells were more sensitive to AMG-102 with IC₅₀ of 14 and 9 μmol/L, respectively. The relative expression levels of c-Met and p-Met proteins in Hep-2 cells were 194.48±0.57 and 177.76±1.53, respectively, which were significantly higher than those in KBV200 cells (171.24±1.00 and 115.37±0.56, respectively, P<0.001 for both). Exogenous hepatocyte growth factor (HGF) was added to increase the expression level of p-Met protein in KBV200 cells. The results showed that AMG-102 significantly reduced the expression of p-Met in KBV200 cells treated with HGF (P<0.001). Compared with the dimethyl sulfoxide (DMSO) group, AMG-102 treatment combined with radiotherapy significantly increased the radiosensitivity of Hep-2 cells (SER=1.28, P<0.001). However, AMG-102 had little effect on the radiosensitivity of KBV200 cells (SER=1.18, P=0.002). Compared with the 4 Gy radiotherapy alone group and the 5 μmol/L of AMG-102 alone treatment group, the apoptosis rate of Hep-2 cells in the combined treatment group was significantly increased. Meanwhile, the expression level of cleaved caspase-3 protein was also markedly increased. However, there were no significant changes in the apoptotic rate and cleaved caspase-3 expression in each treatment group of KBV200 cells. Compared with DMSO treatment group, the expression levels of p-Met, p-Akt and p-Erk were significantly decreased in the 4 Gy radiotherapy group, 5 μmol/L of AMG-102 treatment group and combined treatment group of Hep-2 cells. And the levels of p-Met, p-Akt and p-Erk in the combined treatment group were significantly lower than those in the 4 Gy radiotherapy alone group and 5 μmol/L of AMG-102 treatment alone group. By contrast, in KBV200 cells, the expression of p-Met, p-Akt and p-Erk in each group was not changed. The relative expression of p-Met in Hep-2 cells before and after radiotherapy at 30 min, 1 h, 4 h, 8 h, 24 h were 99.89±0.61, 138.62±1.00, 163.07±5.00, 87.80±1.85, 90.67±0.65 and 94.09±1.41, respectively. The level of p-Met was slightly increased after radiotherapy at 30 min and 1 h (P<0.001 for all), whereas it was significantly decreased from 4 h to 24 h after radiotherapy (P<0.05 for all). By contrast, the expression of p-Met in KBV200 cells did not change with time after radiotherapy (P>0.05). The sensitivity of Hep-2 cells to AMG-102 was decreased after silencing of c-Met, while the sensitivity of KBV200 cells to AMG-102 was not significantly changed (P>0.05). Moreover, the radiosensitivity of Hep-2 cells in c-Met knockdown group had a slightly increasing trend (SER=1.07, P=0.068). After the treatment with 10 μmol/L of AMG-102, the proliferation rate of c-Met ectopically expressed KBV200 cells was 60.05%±3.23%, It was significantly lower than that of the blank control 90.08%±1.04% and siRNA negative control (90.12%±1.01%, P<0.001). The results suggested that the overexpression of c-Met in KBV200 cells increased the radiosensitivity to AMG-102, whereas depletion of c-Met resulted in resistance to AMG-102 in Hep-2 cells. Furthermore, the radiosensitivity of KBV200 cells that overexpressed c-Met showed a decreased trend (SER=0.7, P=0.005). Conclusions c-Met inhibitor AMG-102 has a significant inhibitory effect on the proliferation of c-Met overexpressing laryngeal squamous carcinoma cells, leading to increased radiosensitivity. It suggests that molecular targeted therapy against c-Met receptor is more effective in c-Met overexpressed subtype of laryngeal squamous cell carcinoma.

Objective To investigate the effect of c?Met inhibitor AMG?102 on proliferation and radiosensitivity in laryngeal squamous carcinoma cells. Methods The effects of AMG?102 on proliferation and radiosensitivity of laryngeal squamous carcinoma cell lines Hep?2 and KBV200 were detected by 3?(4,5?dimethy?2?thiazolyl)?2, 5?diphenyl?2H tetrazolium bromide ( MTT ) assay and colony formation assay, respectively. The apoptosis of Hep?2 and KBV200 cells was detected by flow cytometry.The expression levels of c?Met, phospho?Met (p?Met), cleaved caspase?3 and Akt／p?Akt, Erk／p?Erk were detected by Western blot. Specific small interfering RNA targeting c?Met or plasmid of c?Met were transfected into Hep?2 and KBV200 cells to investigate the cell sensitivity to AMG?102. Results Compared with KBV200 cells, Hep?2 cells were more sensitive to AMG?102 with IC50 of 14 and 9 μmol／L, respectively. The relative expression levels of c?Met and p?Met proteins in Hep?2 cells were 194.48±0.57 and 177.76±1.53, respectively, which were significantly higher than those in KBV200 cells ( 171.24 ± 1.00 and 115.37 ± 0.56, respectively, P＜0.001 for both). Exogenous hepatocyte growth factor (HGF) was added to increase the expression level of p?Met protein in KBV200 cells.The results showed that AMG?102 significantly reduced the expression of p?Met in KBV200 cells treated with HGF ( P＜0.001). Compared with the dimethyl sulfoxide ( DMSO) group, AMG?102 treatment combined with radiotherapy significantly increased the radiosensitivity of Hep?2 cells ( SER＝1.28, P＜0.001). However, AMG?102 had little effect on the radiosensitivity of KBV200 cells (SER＝1.18, P＝0.002). Compared with the 4 Gy radiotherapy alone group and the 5 μmol／L of AMG?102 alone treatment group, the apoptosis rate of Hep?2 cells in the combined treatment group was significantly increased. Meanwhile, the expression level of cleaved caspase?3 protein was also markedly increased. However, there were no significant changes in the apoptotic rate and cleaved caspase?3 expression in each treatment group of KBV200 cells. Compared with DMSO treatment group, the expression levels of p?Met, p?Akt and p?Erk were significantly decreased in the 4 Gy radiotherapy group, 5 μmol／L of AMG?102 treatment group and combined treatment group of Hep?2 cells. And the levels of p?Met, p?Akt and p?Erk in the combined treatment group were significantly lower than those in the 4 Gy radiotherapy alone group and 5 μmol／L of AMG?102 treatment alone group. By contrast, in KBV200 cells, the expression of p?Met, p?Akt and p?Erk in each group was not changed. The relative expression of p?Met in Hep?2 cells before and after radiotherapy at 30 min, 1 h, 4 h, 8 h, 24 h were 99.89±0.61, 138.62±1.00, 163.07±5.00, 87.80±1.85, 90.67±0.65 and 94.09±1.41, respectively. The level of p?Met was slightly increased after radiotherapy at 30 min and 1 h (P＜0.001 for all), whereas it was significantly decreased from 4 h to 24 h after radiotherapy (P＜0.05 for all). By contrast, the expression of p?Met in KBV200 cells did not change with time after radiotherapy (P＞0.05). The sensitivity of Hep?2 cells to AMG?102 was decreased after silencing of c?Met, while the sensitivity of KBV200 cells to AMG?102 was not significantly changed ( P＞0.05). Moreover, the radiosensitivity of Hep?2 cells in c?Met knockdown group had a slightly increasing trend ( SER＝1.07, P＝0.068). After the treatment with 10 μmol／L of AMG?102, the proliferation rate of c?Met ectopically expressed KBV200 cells was 60.05%± 3.23%, It was significantly lower than that of the blank control 90.08%±1.04% and siRNA negative control (90.12%±1.01%, P＜0.001). The results suggested that the overexpression of c?Met in KBV200 cells increased the radiosensitivity to AMG?102, whereas depletion of c?Met resulted in resistance to AMG?102 in Hep?2 cells. Furthermore, the radiosensitivity of KBV200 cells that overexpressed c?Met showed a decreased trend (SER＝0.7, P＝0.005). Conclusions c?Met inhibitor AMG?102 has a significant inhibitory effect on the proliferation of c?Met overexpressing laryngeal squamous carcinoma cells, leading to increased radiosensitivity. It suggests that molecular targeted therapy against c?Met receptor is more effective in c?Met overexpressed subtype of laryngeal squamous cell carcinoma.

Objective To investigate the effect of c?Met inhibitor AMG?102 on proliferation and radiosensitivity in laryngeal squamous carcinoma cells. Methods The effects of AMG?102 on proliferation and radiosensitivity of laryngeal squamous carcinoma cell lines Hep?2 and KBV200 were detected by 3?(4,5?dimethy?2?thiazolyl)?2, 5?diphenyl?2H tetrazolium bromide ( MTT ) assay and colony formation assay, respectively. The apoptosis of Hep?2 and KBV200 cells was detected by flow cytometry.The expression levels of c?Met, phospho?Met (p?Met), cleaved caspase?3 and Akt／p?Akt, Erk／p?Erk were detected by Western blot. Specific small interfering RNA targeting c?Met or plasmid of c?Met were transfected into Hep?2 and KBV200 cells to investigate the cell sensitivity to AMG?102. Results Compared with KBV200 cells, Hep?2 cells were more sensitive to AMG?102 with IC50 of 14 and 9 μmol／L, respectively. The relative expression levels of c?Met and p?Met proteins in Hep?2 cells were 194.48±0.57 and 177.76±1.53, respectively, which were significantly higher than those in KBV200 cells ( 171.24 ± 1.00 and 115.37 ± 0.56, respectively, P＜0.001 for both). Exogenous hepatocyte growth factor (HGF) was added to increase the expression level of p?Met protein in KBV200 cells.The results showed that AMG?102 significantly reduced the expression of p?Met in KBV200 cells treated with HGF ( P＜0.001). Compared with the dimethyl sulfoxide ( DMSO) group, AMG?102 treatment combined with radiotherapy significantly increased the radiosensitivity of Hep?2 cells ( SER＝1.28, P＜0.001). However, AMG?102 had little effect on the radiosensitivity of KBV200 cells (SER＝1.18, P＝0.002). Compared with the 4 Gy radiotherapy alone group and the 5 μmol／L of AMG?102 alone treatment group, the apoptosis rate of Hep?2 cells in the combined treatment group was significantly increased. Meanwhile, the expression level of cleaved caspase?3 protein was also markedly increased. However, there were no significant changes in the apoptotic rate and cleaved caspase?3 expression in each treatment group of KBV200 cells. Compared with DMSO treatment group, the expression levels of p?Met, p?Akt and p?Erk were significantly decreased in the 4 Gy radiotherapy group, 5 μmol／L of AMG?102 treatment group and combined treatment group of Hep?2 cells. And the levels of p?Met, p?Akt and p?Erk in the combined treatment group were significantly lower than those in the 4 Gy radiotherapy alone group and 5 μmol／L of AMG?102 treatment alone group. By contrast, in KBV200 cells, the expression of p?Met, p?Akt and p?Erk in each group was not changed. The relative expression of p?Met in Hep?2 cells before and after radiotherapy at 30 min, 1 h, 4 h, 8 h, 24 h were 99.89±0.61, 138.62±1.00, 163.07±5.00, 87.80±1.85, 90.67±0.65 and 94.09±1.41, respectively. The level of p?Met was slightly increased after radiotherapy at 30 min and 1 h (P＜0.001 for all), whereas it was significantly decreased from 4 h to 24 h after radiotherapy (P＜0.05 for all). By contrast, the expression of p?Met in KBV200 cells did not change with time after radiotherapy (P＞0.05). The sensitivity of Hep?2 cells to AMG?102 was decreased after silencing of c?Met, while the sensitivity of KBV200 cells to AMG?102 was not significantly changed ( P＞0.05). Moreover, the radiosensitivity of Hep?2 cells in c?Met knockdown group had a slightly increasing trend ( SER＝1.07, P＝0.068). After the treatment with 10 μmol／L of AMG?102, the proliferation rate of c?Met ectopically expressed KBV200 cells was 60.05%± 3.23%, It was significantly lower than that of the blank control 90.08%±1.04% and siRNA negative control (90.12%±1.01%, P＜0.001). The results suggested that the overexpression of c?Met in KBV200 cells increased the radiosensitivity to AMG?102, whereas depletion of c?Met resulted in resistance to AMG?102 in Hep?2 cells. Furthermore, the radiosensitivity of KBV200 cells that overexpressed c?Met showed a decreased trend (SER＝0.7, P＝0.005). Conclusions c?Met inhibitor AMG?102 has a significant inhibitory effect on the proliferation of c?Met overexpressing laryngeal squamous carcinoma cells, leading to increased radiosensitivity. It suggests that molecular targeted therapy against c?Met receptor is more effective in c?Met overexpressed subtype of laryngeal squamous cell carcinoma.