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Original Research

Long noncoding RNA LINC01296 is associated with poor prognosis in prostate cancer and promotes cancer-cell proliferation and metastasis

, , , , , & show all
Pages 1843-1852 | Published online: 27 Mar 2017

Figures & data

Figure 1 Relative LINC01296 expression in prostate cancer.

Notes: (A) A microarray containing 8277 lncRNA probes was used to identify differentially expressed lncRNAs in three prostate cancer patients. (B) Relative expression of LINC01296 in prostate cancer tissues compared with paired adjacent normal tissues. (C) Relative expression of LINC01296 in prostate cancer cell lines (22Rv1, LNCaP) and normal prostate cell line (WPMY1). Each experiment was repeated three times. **P<0.01.
Abbreviation: lncRNA, long noncoding RNA.
Figure 1 Relative LINC01296 expression in prostate cancer.

Table 1 The association between LINC01296 expression and clinicopathological features of prostate cancer

Figure 2 Kaplan–Meier survival curves of two groups of patients with prostate cancer based on LINC01296-expression levels (P=0.01).

Note: Patients with high levels of LINC01296 expression showed reduced biochemical recurrence-free survival times compared with patients with low levels of LINC01296 expression.
Figure 2 Kaplan–Meier survival curves of two groups of patients with prostate cancer based on LINC01296-expression levels (P=0.01).

Table 2 Cox proportional-hazard model of biochemical recurrence-free survival in prostate cancer

Figure 3 siRNA-mediated knockdown of LINC01296 inhibited prostate cancer-cell proliferation.

Notes: (A) Relative expression levels of LINC01296 in 22Rv1 and LNCaP cells were significantly decreased by siLINC01296 compared with the NC. (B) CCK-8 assays were performed to determine the proliferation of 22Rv1 and LNCaP cells after transfection. (C, D) Colony-formation assays were performed to determine the proliferation of siLINC01296-transfected 22Rv1 and LNCaP cells. Colonies were counted and captured. (EG) Western blot was performed to analyze relative protein-expression levels of the PI3K–Akt–mTOR signaling pathway in siLINC01296-transfected 22Rv1 and LNCaP cells and respective control cells. Data represent mean ± standard deviation from three independent experiments. *P<0.05; **P<0.01.
Abbreviations: siRNA, short interfering RNA; NC, negative control; OD, optical density; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; SI, short interfering RNA1; S2, short interfering RNA2.
Figure 3 siRNA-mediated knockdown of LINC01296 inhibited prostate cancer-cell proliferation.
Figure 3 siRNA-mediated knockdown of LINC01296 inhibited prostate cancer-cell proliferation.

Figure 4 siRNA-mediated knockdown of LINC01296 inhibited prostate cancer-cell migration and invasion.

Notes: Prostate cancer cells transfected with siLINC01296 displayed significantly lower migration (A, B) and invasion (C, D) capacity compared with those transfected with siNC. Data represent mean ± standard deviation from three independent experiments. (EG) Western blot was performed to analyze of vimentin, N-catenin, E-cadherin, and MMP9 protein-expression levels in siLINC01296-transfected 22Rv1 and LNCaP cells and respective control cells. Data represent mean ± standard deviation from three independent experiments. *P<0.05.
Abbreviations: siRNA, short interfering RNA; NC, negative control; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; SI, short interfering RNA1; S2, short interfering RNA2.
Figure 4 siRNA-mediated knockdown of LINC01296 inhibited prostate cancer-cell migration and invasion.