Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: Expression analysis of MIR137HG in GC patients. A QRT-PCR analysis of MIR137HG expression in 69 paired gastric cancer (GC) and surgical margin (SM) samples (Paired t-test: P = 0.037); B Compration the expression of MIR137HG in SM samples between GC patients with poor differentiation and moderate/ well differentiation (Mann–Whitney U -test: P = 0.003); C Compration the expression of MIR137HG in GC samples between male patients and female patients (Mann–Whitney U -test: P = 0.039); D ROC curve used for discriminating GC patients with with poor differentiation from moderate/ well differentiation( AUC = 66.9%, Cutoff value = 0.07, P = 0.042)

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Expressing, Quantitative RT-PCR, MANN-WHITNEY

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: Construction of MIR137HG over-expression cell lines and the colony formation assay. A and B Construction of MIR137HG over-expression cell lines ( A a and b BGC823 Ctrl and MIR137HG, P = 0.001; B a and b HGC27 Ctrl and MIR137HG, P = 0.002). C and D Colony formation assay ( C a and b BGC823 Ctrl and MIR137HG, P = 0.005; D a and b HGC27 Ctrl and MIR137HG, P = 0.084)

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Over Expression, Colony Assay

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: Transwell and Scratch assays. A and B Transwell assay ( A (a,b,c): BGC823 Ctrl and MIR137HG, P < 0.001; B (a,b,c): HGC27 Ctrl and MIR137HG, P = 0.005). C and D Scratch assay ( C (a,b,c): BGC823 Ctrl and MIR137HG, P < 0.001; D (a,b,c), HGC27 Ctrl and MIR137HG, P = 0.020)

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Transwell Assay, Wound Healing Assay

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: The relationship between miR-2682-3p and MIR137HG. A UCSC database indicated the gene location of miR-137, miR-2682, and MIR137HG. Data showed that miR-2682 was embedded at the second intron of gene MIR137HG, while miR-137 was embedded at the third exon of gene MIR137HG B The expression relationship among MIR137HG, miR-137, and miR-2682-3p was tested by QRT-PCR. Data showed that MIR137HG was positively related to miR-137 ( P = 0.004), while it was negatively related to miR-2682-3p ( P = 0.001). C and D showed the colony formation assays. Data showed that miR-2682-3p mimic could inhibit the colony formation of BGC823 MIR137HG ( P = 0.02), while miR-2682-3p inhibitor could promote the colony formation of BGC823 Ctrl ( P = 0.002)

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Expressing, Quantitative RT-PCR

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: The function of miR-2682-3p and MIR137HG on the migration ability of BGC823. A and B The scratch assay indicated that miR-2682-3p mimic could inhibit the migration ability of BGC823 MIR137HG ( P = 0.066), while miR-2682-3p inhibitor could promote the migration ability BGC823 Ctrl ( P = 0.032). C and D The transwell assay indicated miR-2682-3p mimic could inhibit the migration ability of BGC823 MIR137HG ( P = 0.002), while miR-2682-3p inhibitor could promote the migration ability of BGC823 Ctrl ( P = 0.015)

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Migration, Wound Healing Assay, Transwell Assay

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: Animal models in nude mice. A Photographs of xenograft tumors after sacrifice: Ctrl VS MIR137HG; B Weight of xenograft tumors ( n = 3, P = 0.001); C Representative photographs of immunohistochemical staining of KI67 and FUS in xenograft tumors. (Scale bar = 50 μm). D Photographs of xenograft tumors formed by intratumoral injection after sacrifice (Ago-miR-NC VS Ago-miR-2682-3p). E Final volume weight of xenograft tumors formed by intratumoral injection ( n = 3, P = 0.035); F Comparing the growth rate of tumor volume treated by Ago-miR-NC and Ago-miR-2682-3p. G Photograph of lung metastasis tumors after sacrifice (MIR137HG VS Ctrl, 2/3 VS 1/3)

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Immunohistochemical staining, Staining, Injection

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: The subcellular location of MIR137HG and the interaction among molecules. A The subcellular location of MIR137HG BGC823; B The subcellular location of MIR137HG HGC27 ( DAPI was used to stain the nucleus; Cy3 separately labeled MIR137HG, U6, and 18S; U6 was the control of nucleus sub-location; 18S was the control of cytoplasm); C Starbase V2.0 indicated that FUS was a candidate target of MIR137HG; D RIP assay showed that FUS could directly interact with MIR137HG; E Con-focus data showed that MIR137HG and FUS could sub-locate in the same region of the cell; F TargetScan predicted that miR-2682-3p could target with FUS; G The String database predicted the relationships among FUS and its candidated targets tested by IP followed LC-MS/MS; H Western blot data showed that miR-2682-3p mimic could inhibit the expression of FUS in BGC823 MIR137HG, while miR-2682-3p inhibitor could promote the expression of FUS in BGC823 Ctrl; I Dual-luciferase assay showed that miR-2683-3p could bind data showed that MET and RHOC could co-express with FUS; J Western blot data showed the expression of MET, CTNNB1, RHOC, ACTB (ACTIN labelled in the primary gel picture), FUS in BGC823 Ctrl and BGC823 MIR137HG

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Staining, Labeling, Control, Liquid Chromatography with Mass Spectroscopy, Western Blot, Expressing, Luciferase

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: Structure chart of the role of the MIR137HG/FUS/miR-2682-3p axis in gastric cancer progression. Our combined data indicated a model whereby MIR137HG promotes the advancement of gastric cancer through interacting with FUS, followed by influencing a series downstream related proteins (MET, RHOC, CTNNB1) and finally affecting GC progression. miR-2682-3p could inhibit the function of MIR137HG by targeting FUS

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques:

Journal: BMC Cancer

Article Title: miR-2682-3p antagonizes its host lncRNA-MIR137HG by interacting with the same target FUS to regulate the progression of gastric cancer

doi: 10.1186/s12885-022-09740-9

Figure Lengend Snippet: Clinical features of MIR137HG expression in gastric cancer samples and paired surgical margin samples

Article Snippet: About 2 × 10 7 BGC823 MIR137HG cell strain was washed with pre-chilled phosphate-buffered saline (PBS) and lysed by RIPA (R0010-20, Solarbio, China).

Techniques: Expressing

Journal: Clinical and Translational Medicine

Article Title: Exosome‐transmitted miR‐769‐5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53

doi: 10.1002/ctm2.780

Figure Lengend Snippet: miR‐769‐5p is enriched in BGC823/DDP cell‐derived exosomes. (A) Double‐membrane exosomes purified from the supernatants of BGC823 and BGC8231/DDP cells were observed by transmission electron microscopy (TEM). (B) NanoSight particle tracking analysis (NTA) of the diameter and concentration of vesicles(particles/ml). (C and D) Exosomal markers TSG101, CD9, CD81 and CD63 were detected by Western blot and FCM to prove that the extract in exosomal protein purified from cell supernatants has the typical characteristics of exosomes. (E and F) Cluster heat map and Volcano plot of differential miRNAs in exosomes purified from the supernatants of BGC823 and BGC823/DDP cells. (G) qRT‐PCR verified the relative expression of miR‐769‐5p in exosomes purified from the supernatants of BGC823, BGC823/DDP, SGC7901 and SGC7901/DDP cells. (H) Different expression of miR‐769‐5p between 41 pairs of tumour and adjacent tumour, 41 tumours and 346 adjacent tumours according to TCGA database. (I and J) The positive rate (referring to the percentage of positive cells with red staining) of miR‐769‐5p in 75 pairs of gastric cancer tissues and adjacent tissues by RNA in situ hybridisation (ISH). (K) qRT‐PCR detected the relative expression of miR‐769‐5p in serum exosomes of 60 cases (including 41 cisplatin‐sensitive cases and 19 cisplatin‐resistant cases) of GC patients. The level of serum miR‐769‐5p was significantly increased in non‐response patients ( n 1 = 19) compared with response patients ( n 2 = 41). Quantitative data from three independent experiments are shown as the mean ± SD (error bars). * p < .05, ** p < .01, *** p < .001 (Student's t ‐test)

Article Snippet: Through RNA‐seq, the level of miR‐769‐5p expressed in BGC823/DDP secreted exosomes (BD Exo) was 4.77 times that in BGC secreted exosomes (BC Exo) (Figure ).

Techniques: Derivative Assay, Purification, Transmission Assay, Electron Microscopy, Concentration Assay, Western Blot, Quantitative RT-PCR, Expressing, Staining, In Situ, Hybridization

Journal: Clinical and Translational Medicine

Article Title: Exosome‐transmitted miR‐769‐5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53

doi: 10.1002/ctm2.780

Figure Lengend Snippet: Exosome‐mediated transfer of miR‐769‐5p is required for GC cisplatin‐resistance and targets CASP9 directly. (A) The survival of BGC823 or SGC7901 cells co‐cultured with BD Exo or SD Exo (200 μg/ml) for 24 h and treated with cisplatin for 24 h was detected by CCK‐8. (B) The rates of BGC823 cells’ apoptosis were reduced after being co‐cultured with BD Exo (200ug/ml) for 24 h and treated with cisplatin (0.4 μg/ml) for 24 h detected by FCM. (C) Red fluorescence was observed in the BGC823 or SGC7901 cells after co‐cultured with BGC823/DDP or SGC7901/DDP cells which were transfected with the Cy3‐miR‐769‐5p mimic (red fluorescence) for 48 h. (D) Confocal microscopy showed internalisation of exosomes in BGC823 or SGC7901 recipient cells after co‐cultured with PKH26‐labeled (red fluorescence) BD Exo or SD Exo for 24 h. DAPI was used to stain the nuclei of BGC823 or SGC7901 recipient cells with blue fluorescence. (E) qRT‐PCR showed the expression of miR‐769‐5p in in BGC anti‐NC + PBS, BGC anti‐NC + BD Exo and BGC anti‐769 + BD Exo. (F) Luciferase reporter was carried out in HEK293T co‐transducted with miR‐769‐5p‐mimics or miRNA control with firefly luciferase reporter plasmid containing either wild‐type (WT) or mutant (MUT) CASP9 3′UTR (pGL3‐CASP9‐WT or pGL3‐CASP9‐MUT). (G) Predicted binding sites of the CASP9 3′UTR by miR‐769‐5p. (H and I) PCR and Western blot confirmed that miR‐769‐5p negatively regulated the expression of CASP9. (J and K) The mRNA and protein levels of CASP9 in BGC anti‐NC + PBS, BGC anti‐NC + BD Exo and BGC anti‐769 + BD Exo. (L) qRT‐PCR showed the expression of miR‐769‐5p in BGC + BD Exo DMSO and BGC + BD Exo GW4869. (M and N) qRT‐PCR and Western blot showed the expression of CASP9 in BGC + BD Exo DMSO and BGC + BD Exo GW4869. (N and O) The up‐regulation of CASP9 mRNA and protein was detected by qRT‐PCR and Western blot in BGC + BD anti‐769 Exo. Quantitative data from three independent experiments are shown as the mean ± SD (error bars). * p < .05, ** p < .01, *** p < .001 (Student's t ‐test)

Article Snippet: Through RNA‐seq, the level of miR‐769‐5p expressed in BGC823/DDP secreted exosomes (BD Exo) was 4.77 times that in BGC secreted exosomes (BC Exo) (Figure ).

Techniques: Cell Culture, CCK-8 Assay, Fluorescence, Transfection, Confocal Microscopy, Labeling, Staining, Quantitative RT-PCR, Expressing, Luciferase, Plasmid Preparation, Mutagenesis, Binding Assay, Western Blot

Journal: Clinical and Translational Medicine

Article Title: Exosome‐transmitted miR‐769‐5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53

doi: 10.1002/ctm2.780

Figure Lengend Snippet: Exosomal miR‐769‐5p confers cisplatin resistance through down‐regulating CASP9 along with subsequent evasion of apoptosis and confirmed in vivo. (A) Western blot analysis of caspase9, caspase3 and cleaved caspase3 in BGC anti‐NC + PBS, BGC anti‐NC + BD Exo, BGC anti‐769 + BD Exo and BGC CASP9 + BD Exo. (B) Western blot analysis of caspase9, caspase3 and cleaved caspase3 in BGC + BD Exo DMSO and BGC + BD Exo GW4869. (C) Western blot analysis of caspase9, caspase3 and cleaved caspase3 in BGC + BD anti‐NC Exo, BGC + BD anti‐769 Exo and BGC + BD anti‐769 + siCASP9 Exo. (D) Subcutaneous xenograft assay of BGC823 cells with or without BD Exo (200 μg/100 μl cells per mouse) once every 2 days in nude mice with PBS or cisplatin (DDP, 4 mg/kg) treatment. (E) Tumour volume of xenograft models were measured every 3 days and shown. Tumour volume (mm 3 ) = 0.5 × width 2 × length. (F) Tumour weight of xenograft models were measured every 3 days and shown. (G) CASP9, cleaved caspase3 and p53 expression levels were shown in representative xenograft tumours by Immunohistochemistry (IHC) (400× magnification, scale bars = 50 μm). Results are presented as mean ± SD. * p < .05, ** p < .01, *** p < .001

Article Snippet: Through RNA‐seq, the level of miR‐769‐5p expressed in BGC823/DDP secreted exosomes (BD Exo) was 4.77 times that in BGC secreted exosomes (BC Exo) (Figure ).

Techniques: In Vivo, Western Blot, Xenograft Assay, Expressing, Immunohistochemistry

Journal: Clinical and Translational Medicine

Article Title: Exosome‐transmitted miR‐769‐5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53

doi: 10.1002/ctm2.780

Figure Lengend Snippet: Exosomal miR‐769‐5p induces cisplatin resistance and promotes the tumorigenesis of GC in vivo. (A) Subcutaneous xenograft assay of BGC823/DDP cells (5 × 10 6 cells/100 μl) with or without miR‐769‐5p knockdwon in nude mice with PBS or cisplatin (DDP, 4 mg/kg) treatment. (B) Tumour volume of xenograft models were measured every 3 days and shown. (C) Tumour weight of xenograft models were measured every 3 days and shown. (D) Levels of exosomal miR‐769‐5p in the serum were detected by qPCR. (E) CASP9, cleaved caspase3 and p53 expression levels were shown in representative xenograft tumours by immunohistochemistry (IHC) (400× magnification, scale bars = 50 μm). (F) Subcutaneous xenograft assay of BGC823 cells (5 × 10 6 cells/100 μl) with or without miR‐769‐5p overexpressed in nude mice with PBS or cisplatin (DDP, 4 mg/kg) treatment. (G) Tumour volume of xenograft models were measured every 3 days and shown. (H) Tumour weight of xenograft models were measured every 3 days and shown. (I) Levels of exosomal miR‐769‐5p in the serum were detected by qPCR. (J) Caspase9, cleaved caspase3 and p53 expression levels were shown in representative xenograft tumours by Immunohistochemistry (IHC) (400× magnification, scale bars = 50 μm). (K) Summary of the mechanism by which exosomal miR‐769‐5p induces cisplatin resistance. Results are presented as mean SD. * p < .05, ** p < .01, *** p < .001

Article Snippet: Through RNA‐seq, the level of miR‐769‐5p expressed in BGC823/DDP secreted exosomes (BD Exo) was 4.77 times that in BGC secreted exosomes (BC Exo) (Figure ).

Techniques: In Vivo, Xenograft Assay, Expressing, Immunohistochemistry

Journal: Cancer Cell International

Article Title: Promotion of gastric tumor initiating cells in a 3D collagen gel culture model via YBX1/SPP1/NF-κB signaling

doi: 10.1186/s12935-021-02307-x

Figure Lengend Snippet: Collagen gels mediated TICs characteristics through ITGB1 signaling in gastric cancer. A Relative expression of ITGB1–8 in SGC-7901/BGC-823 cells cultured in dish or 3D gels, which was determined by real-time quantitative PCR. B Western blotting of ITGB1 in SGC-7901/BGC-823 cells cultured in dish or 3D gels. C Western blotting of ITGB1 in SGC-7901/BGC-823 (SCR) and ITGB1 KO SGC-7901/BGC-823 (KO1, KO2). D The colony growth curve of SGC-7901/BGC-823 and ITGB1 KO SGC-7901/BGC-823 cells in 3D collagen gels. The scale bar is 50 μm. E The cell apoptosis of SGC-7901/BGC-823 and ITGB1 KO SGC-7901/BGC-823 cells in 3D collagen gels on day 5. F SGC-7901/BGC-823 and ITGB1 KO SGC-7901/BGC-823 cells were cultured in 3D collagen gels for 5 days. Then tumor cells were collected and the colony formation capability was examined. G Tumor cells in ( F ) were collected and the tumorigenic capability was examined in mice. 10 5 SGC-7901 or BGC-823 cells were subcutaneously injected into NOD-SCID mice (n = 10 in each group, day 30). The tumor diameter > 1 mm were determined as tumorigenicity. The percentage of mice with tumorigenicity in 10 mice was determined as tumorigenesis rate. H Tumor cells in ( F ) were collected and the cell migration was examined by transwell (24 h). I Tumor cells in ( F ) were collected and treated with 5-FU (1 µg/ml) for 48 h. The cell apoptosis was examined using Annexin/PI staining. J Tumor cells in ( F ) were collected and treated with PTX (2 µg/ml) for 48 h. The cell apoptosis was examined using Annexin/PI staining. K Immunohistochemical staining of ITGB1 in gastric tumor tissues from high stage (H-S, stage T3–4) and low stage (L-S, stage T1–2) patients (n=10 in each group). The scale bar is 50 μm. L Overall survival of gastric cancer patients with high/low ITGB1 expression (low expression, n= 95 and high expression, n= 297)

Article Snippet: The ITGB1, SPP1 and YBX1 knockdown SGC-7901/BGC-823 cells were purchased from Cyagen (China) and the knockdown efficiency was determined by western blotting.

Techniques: Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Western Blot, Injection, Migration, Staining, Immunohistochemical staining

Journal: Cancer Cell International

Article Title: Promotion of gastric tumor initiating cells in a 3D collagen gel culture model via YBX1/SPP1/NF-κB signaling

doi: 10.1186/s12935-021-02307-x

Figure Lengend Snippet: ITGB1 regulated TICs characteristics through YBX1/SPP1 signaling. A Western blotting of YBX1 and SPP1 in SGC-7901/BGC-823 (Dish), 3D cultured SGC-7901/BGC-823 and 3D cultured ITGB1 KO SGC-7901/BGC-823 cells (KO1, KO2). B Western blotting of YBX1 in SGC-7901/BGC-823 (SCR) and YBX1 KO SGC-7901/BGC-823 cells (KO1, KO2). C Western blotting of SPP1 in SGC-7901/BGC-823 (SCR) and SPP1 KO SGC-7901/BGC-823 cells (KO1, KO2). D The colony growth curves of SGC-7901/BGC-823 and YBX1 KO SGC-7901/BGC-823 cells in 3D collagen gels. The scale bar is 50 μm. E The colony growth curves of SGC-7901/BGC-823 and SPP1 KO SGC-7901/BGC-823 cells in 3D collagen gels. The scale bar is 50 μm. F The colony formation capability of SGC-7901/BGC-823 and YBX1 KO SGC-7901/BGC-823 cells in dish. G The colony formation capability of SGC-7901/BGC-823 and SPP1 KO SGC-7901/BGC-823 cells in dish. H SGC-7901/BGC-823, YBX1 KO SGC-7901/BGC-823 and SPP1 KO SGC-7901/BGC-823 cells were collected and treated with 5-FU (1 µg/ml) for 48 h. The cell apoptosis was examined using Annexin/PI staining. I SGC-7901/BGC-823, YBX1 KO SGC-7901/BGC-823 and SPP1 KO SGC-7901/BGC-823 cells were collected and treated with PTX (2 µg/ml) for 48 h. The cell apoptosis was examined using Annexin/PI staining. J overall survival of gastric cancer patients with high/lowYBX1 expression (low expression, n = 173 and high expression, n = 172). K overall survival of gastric cancer patients with high/low SPP1 expression (low expression, n = 169 and high expression, n = 172)

Article Snippet: The ITGB1, SPP1 and YBX1 knockdown SGC-7901/BGC-823 cells were purchased from Cyagen (China) and the knockdown efficiency was determined by western blotting.

Techniques: Western Blot, Cell Culture, Staining, Expressing

Journal: Cancer Cell International

Article Title: Promotion of gastric tumor initiating cells in a 3D collagen gel culture model via YBX1/SPP1/NF-κB signaling

doi: 10.1186/s12935-021-02307-x

Figure Lengend Snippet: Blockade of ITGB1/ NF-κB signals revealed improved outcome in gastric cancer therapy. A Tumor volumes of SGC-7901 bearing mice treated with PBS, LDV, PTX and LDV combining PTX. B Survival time of SGC-7901 bearing mice treated with PBS, LDV, PTX and LDV combining PTX. C Tumor volumes of 3D collagen cultured SGC-7901 bearing mice treated with PBS, LDV, PTX and LDV combining PTX. D Survival time of 3D collagen cultured SGC-7901 bearing mice treated with PBS, LDV, PTX and LDV combining PTX. E Immunofluorescence of ITGB1 and NF-κB in tumor tissues from SGC-7901 bearing mice and 3D collagen cultured SGC-7901 bearing mice on day 15. The scale bar is 50 μm. F immunofluorescence of ITGB1 and NF-κB in tumor tissues from 3D collagen cultured SGC-7901 bearing mice on day 30 (treated with PBS, LDV, PTX, LDV combining PTX). The scale bar is 50 μm. G Tumor volumes of 3D collagen cultured SGC-7901 bearing mice treated with PBS, JSH-23, PTX and JSH-23 combining PTX. H Survival time of 3D collagen cultured SGC-7901 bearing mice treated with PBS, JSH-23, PTX and JSH-23 combining PTX

Article Snippet: The ITGB1, SPP1 and YBX1 knockdown SGC-7901/BGC-823 cells were purchased from Cyagen (China) and the knockdown efficiency was determined by western blotting.

Techniques: Cell Culture, Immunofluorescence