Backgroud: The leading cause of death in pancreatic cancer (PC) patients is the progression of cancer metastasis. Long non-coding RNAs (lncRNAs) play an important role in regulating cancers, however its molecular basis in pancreatic cancer (PC) remains to be explored.
Methods: In this study, bioinformatics methods are used to predict the potential pairs of lncRNAs in PC. The clinical significance of LINC01094 are determined by qRT-PCR and explored its correlation with clinicopathological parameters. The biological functions and potential mechanisms of LINC01094 in PC progression are studied in vivo and in vitro.
Results: We observe that LINC01094 is markedly overexpressed in pancreatic tumors and is associated with poorer prognosis. Downregulation of LINC01094 decreases PC cell invasion and inhibits tumorigenesis and metastasis in mouse xenografts. LINC01094 acts as a sponge for miR-577, sequestering it and derepressing the expression of its endogenous target the RNA‐binding protein lin‐28 homolog B (LIN28B).
Conclusions: Overall, LINC01094 upregulates LIN28B by sponging miR-577, thereby promoting PC proliferation and metastasis. This indicates that LINC01094 can be regarded as a new biomarker or therapeutic target for the treatment of PC.

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This is a list of supplementary files associated with this preprint. Click to download.
Supplementary Table S1 The target sites of shRNA and all primers used for PCR amplification are shown.
Supplementary Table S2 Potential miRNAs associated with LINC01094 were predicted from starBase.
Supplementary Fig. S1 LINC01094 expression levels is decreased after transfection with the corresponding siRNA plasmids. (A) The changes in LINC01094 expression levels were evaluated by qRT-PCR analysis. (B) Representative images of PANC-1 cells transfected with shNC and shLINC01094, respectively (**p<0.01); data were expressed as mean±SD and analyzed using unpaired t-test. The experiment was repeated three times.
Supplementary Fig. S2 Overexpression of LINC01094 promotes PC cells proliferation, invasion and migration in vitro. (A) qRT-PCR was used to detect LINC01094 expression in CFPAC-1 cells stably transfected with vector and LINC01094. (B-C) PC cell proliferation was measured using colony formation and EdU assays in stable LINC01094 overexpression cells compared with the vector control (**p<0.01, scale bar, 100 μm). (D-E) PC cell invasion and migration were measured using wound healing and transwell assays in stable LINC01094 overexpression cells compared with the Vector control (**p<0.01, scale bar, 100 μm); data were expressed as mean±SD and analyzed using unpaired t-test. The experiment was repeated three times.
Supplementary Fig. S3 LIN28B is key for LINC01094-mediated PC cell proliferation and metastasis. (A) Western blot was used to detect LIN28B, MMP9, and PANC expression in CFPAC-1 cells stably co-transfected with LINC01094 and shLIN28B. (B-C) PC cell proliferation was measured using colony formation and EdU assays in stably co-transfected with LINC01094 and shLIN28B (**p<0.01, scale bar, 100 μm). (D-E) PC cell invasion and migration were measured using wound healing and transwell assays in stably co-transfected with LINC01094 and shLIN28B (**p<0.01, scale bar, 100 μm); those among multiple groups were analyzed by the one-way ANOVA or repeated-measures ANOVA.
Supplementary Fig. S4 The heat map shows differentially expressed lncRNA in GSE7189 and GSE15471 GEO datasets.
Supplementary Fig. S5 The heat map shows differentially expressed lncRNA in GSE102238-A GEO datasets.
Supplementary Fig. S6 The heat map shows differentially expressed lncRNA in GSE102238-B GEO datasets.
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Posted 05 Jan, 2021
Posted 05 Jan, 2021
Backgroud: The leading cause of death in pancreatic cancer (PC) patients is the progression of cancer metastasis. Long non-coding RNAs (lncRNAs) play an important role in regulating cancers, however its molecular basis in pancreatic cancer (PC) remains to be explored.
Methods: In this study, bioinformatics methods are used to predict the potential pairs of lncRNAs in PC. The clinical significance of LINC01094 are determined by qRT-PCR and explored its correlation with clinicopathological parameters. The biological functions and potential mechanisms of LINC01094 in PC progression are studied in vivo and in vitro.
Results: We observe that LINC01094 is markedly overexpressed in pancreatic tumors and is associated with poorer prognosis. Downregulation of LINC01094 decreases PC cell invasion and inhibits tumorigenesis and metastasis in mouse xenografts. LINC01094 acts as a sponge for miR-577, sequestering it and derepressing the expression of its endogenous target the RNA‐binding protein lin‐28 homolog B (LIN28B).
Conclusions: Overall, LINC01094 upregulates LIN28B by sponging miR-577, thereby promoting PC proliferation and metastasis. This indicates that LINC01094 can be regarded as a new biomarker or therapeutic target for the treatment of PC.

Figure 1

Figure 2

Figure 3

Figure 4

Figure 5

Figure 6

Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
Supplementary Table S1 The target sites of shRNA and all primers used for PCR amplification are shown.
Supplementary Table S2 Potential miRNAs associated with LINC01094 were predicted from starBase.
Supplementary Fig. S1 LINC01094 expression levels is decreased after transfection with the corresponding siRNA plasmids. (A) The changes in LINC01094 expression levels were evaluated by qRT-PCR analysis. (B) Representative images of PANC-1 cells transfected with shNC and shLINC01094, respectively (**p<0.01); data were expressed as mean±SD and analyzed using unpaired t-test. The experiment was repeated three times.
Supplementary Fig. S2 Overexpression of LINC01094 promotes PC cells proliferation, invasion and migration in vitro. (A) qRT-PCR was used to detect LINC01094 expression in CFPAC-1 cells stably transfected with vector and LINC01094. (B-C) PC cell proliferation was measured using colony formation and EdU assays in stable LINC01094 overexpression cells compared with the vector control (**p<0.01, scale bar, 100 μm). (D-E) PC cell invasion and migration were measured using wound healing and transwell assays in stable LINC01094 overexpression cells compared with the Vector control (**p<0.01, scale bar, 100 μm); data were expressed as mean±SD and analyzed using unpaired t-test. The experiment was repeated three times.
Supplementary Fig. S3 LIN28B is key for LINC01094-mediated PC cell proliferation and metastasis. (A) Western blot was used to detect LIN28B, MMP9, and PANC expression in CFPAC-1 cells stably co-transfected with LINC01094 and shLIN28B. (B-C) PC cell proliferation was measured using colony formation and EdU assays in stably co-transfected with LINC01094 and shLIN28B (**p<0.01, scale bar, 100 μm). (D-E) PC cell invasion and migration were measured using wound healing and transwell assays in stably co-transfected with LINC01094 and shLIN28B (**p<0.01, scale bar, 100 μm); those among multiple groups were analyzed by the one-way ANOVA or repeated-measures ANOVA.
Supplementary Fig. S4 The heat map shows differentially expressed lncRNA in GSE7189 and GSE15471 GEO datasets.
Supplementary Fig. S5 The heat map shows differentially expressed lncRNA in GSE102238-A GEO datasets.
Supplementary Fig. S6 The heat map shows differentially expressed lncRNA in GSE102238-B GEO datasets.
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