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LIN28B promotes colon cancer migration and recurrence.

Pang M, Wu G, Hou X, Hou N, Liang L, Jia G, Shuai P, Luo B, Wang K, Li G - PLoS ONE (2014)

Bottom Line: LIN28B is involved in "stemness" and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members.LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence.In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.

ABSTRACT
LIN28B is involved in "stemness" and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members. In this study, we showed that LIN28B expression promotes migration and recurrence of colon cancer. Immunohistochemistry and reverse-transcription polymerase chain reactions were performed to detect LIN28B expression in colon cancer tissue microarrays, paraffin-embedded surgical resected tissues and cancer cells. Loss-of-function, migration and proliferation analyses were performed to delineate the potential roles of LIN28B in colon cancer. LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence. LIN28B suppression inhibited the migration of SW480 colon cancer cells and facilitated the cytotoxicity induced by oxaliplatin in SW480 and HCT116 colon cancer cells. In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.

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si-LIN28B efficiently inhibited the expression of LIN28B in HCT116 and SW480 cells.(A–B) RT-PCR and Western blot analyses confirmed the efficiency of sh-LIN28B knockdown in HCT116 and SW480 cells. (C–D) A qRT-PCR analysis also confirmed the downregulation of LIN28B mRNA in these cells. The data are represented as the mean ± SE (n = 3; Student's t-test).
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pone-0109169-g004: si-LIN28B efficiently inhibited the expression of LIN28B in HCT116 and SW480 cells.(A–B) RT-PCR and Western blot analyses confirmed the efficiency of sh-LIN28B knockdown in HCT116 and SW480 cells. (C–D) A qRT-PCR analysis also confirmed the downregulation of LIN28B mRNA in these cells. The data are represented as the mean ± SE (n = 3; Student's t-test).

Mentions: The let-7 tumour suppressor microRNA family members are known to regulate chemosensitivity [17], while LIN28B promotes malignancy mainly by inhibiting let-7 biogenesis. Thus, we sought to determine whether LIN28B could influence chemosensitivity to oxaliplatin. We examined LIN28B expression in three colon cancer cell lines using RT-PCR and Western blotting (Fig. 3A). HCT116 and SW480 cells were selected for use in these experiments due to their low and high level of Lin28 expression, respectively. Oxaliplatin induced concentration-dependent cytotoxicity in these cells (Fig. 3B). The IC50 value for oxaliplatin was 6.23±0.75 µg/mL for the HCT116 cells, and this was increased by 30% to 10.7±2.26 µg/mL in the SW480 cells. This finding suggested that differences in LIN28B expression may serve to modulate chemosensitivity in colon cancer cells. To verify this hypothesis, we constructed LIN28B-specific siRNA and control small RNA. The efficiency of the si-LIN28B was determined in both cell lines (Fig. 4A–D), and then a CCK-8 analysis was performed to explore the interactions between the si-LIN28B and oxaliplatin in HCT116 and SW480 cells. The results indicated a synergistic effect between si-LIN28B and oxaliplatin (Fig. 3C–D), which suggests that the targeting of LIN28B may be capable of sensitising colon cancer cells to oxaliplatin therapy.


LIN28B promotes colon cancer migration and recurrence.

Pang M, Wu G, Hou X, Hou N, Liang L, Jia G, Shuai P, Luo B, Wang K, Li G - PLoS ONE (2014)

si-LIN28B efficiently inhibited the expression of LIN28B in HCT116 and SW480 cells.(A–B) RT-PCR and Western blot analyses confirmed the efficiency of sh-LIN28B knockdown in HCT116 and SW480 cells. (C–D) A qRT-PCR analysis also confirmed the downregulation of LIN28B mRNA in these cells. The data are represented as the mean ± SE (n = 3; Student's t-test).
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4215835&req=5

pone-0109169-g004: si-LIN28B efficiently inhibited the expression of LIN28B in HCT116 and SW480 cells.(A–B) RT-PCR and Western blot analyses confirmed the efficiency of sh-LIN28B knockdown in HCT116 and SW480 cells. (C–D) A qRT-PCR analysis also confirmed the downregulation of LIN28B mRNA in these cells. The data are represented as the mean ± SE (n = 3; Student's t-test).
Mentions: The let-7 tumour suppressor microRNA family members are known to regulate chemosensitivity [17], while LIN28B promotes malignancy mainly by inhibiting let-7 biogenesis. Thus, we sought to determine whether LIN28B could influence chemosensitivity to oxaliplatin. We examined LIN28B expression in three colon cancer cell lines using RT-PCR and Western blotting (Fig. 3A). HCT116 and SW480 cells were selected for use in these experiments due to their low and high level of Lin28 expression, respectively. Oxaliplatin induced concentration-dependent cytotoxicity in these cells (Fig. 3B). The IC50 value for oxaliplatin was 6.23±0.75 µg/mL for the HCT116 cells, and this was increased by 30% to 10.7±2.26 µg/mL in the SW480 cells. This finding suggested that differences in LIN28B expression may serve to modulate chemosensitivity in colon cancer cells. To verify this hypothesis, we constructed LIN28B-specific siRNA and control small RNA. The efficiency of the si-LIN28B was determined in both cell lines (Fig. 4A–D), and then a CCK-8 analysis was performed to explore the interactions between the si-LIN28B and oxaliplatin in HCT116 and SW480 cells. The results indicated a synergistic effect between si-LIN28B and oxaliplatin (Fig. 3C–D), which suggests that the targeting of LIN28B may be capable of sensitising colon cancer cells to oxaliplatin therapy.

Bottom Line: LIN28B is involved in "stemness" and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members.LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence.In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.

ABSTRACT
LIN28B is involved in "stemness" and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members. In this study, we showed that LIN28B expression promotes migration and recurrence of colon cancer. Immunohistochemistry and reverse-transcription polymerase chain reactions were performed to detect LIN28B expression in colon cancer tissue microarrays, paraffin-embedded surgical resected tissues and cancer cells. Loss-of-function, migration and proliferation analyses were performed to delineate the potential roles of LIN28B in colon cancer. LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence. LIN28B suppression inhibited the migration of SW480 colon cancer cells and facilitated the cytotoxicity induced by oxaliplatin in SW480 and HCT116 colon cancer cells. In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.

Show MeSH
Related in: MedlinePlus