<i>LRRC3B</i>, Encoding a Leucine-Rich Repeat-Containing Protein, Is a Putative Tumor Suppressor Gene in Gastric Cancer

Kim, Mirang; Kim, Jeong‐Hwan; Jang, Hay-Ran; Kim, Hwan‐Mook; Lee, Chang-Woo; Noh, Seung Man; Song, Kyu‐Sang; Cho, June-Sik; Kim, Jeong Il; Hahn, Yoonsoo; Yeom, Young‐Il; Yoo, Hyang–Sook; Kim, Yong‐Sung

doi:10.1158/0008-5472.can-08-0667

Cited by 49 publications

(43 citation statements)

References 43 publications

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“…LRRC3B has been reported to be a tumor suppressor for gastric cancer (24), and Tian et al (25) revealed the tumor suppressor role of LRRC3B in colorectal cancer using a gene silencing method. The role of LRRC3B in breast cancer has not been fully discussed, even in primary breast cancer surgery.…”

Section: Discussionmentioning

confidence: 99%

“…An increasing number of studies have mentioned the pivotal role of LRRC3B in tumor development and progression. For instance, Kim et al (15) reported that LRRC3B was a tumor suppressor for gastric cancer. Furthermore, LRRC3B was downregulated in a renal cell carcinoma line, which suggests that LRRC3B could be involved in the process of carcinogenesis as a tumor suppressor (13,16).…”

Section: Introductionmentioning

confidence: 99%

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Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Kong

Zou

2017

Oncology Letters

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Abstract. The present study aimed to investigate the potential effect of leucine-rich repeat containing 3B (LRRC3B) with respect to the inhibition of breast cancer recurrence and metastasis post-anesthesia. The mRNA expression of LRRC3B in breast MDA-MB-231 and MCF-7 cell lines was detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. The effect of bupivacaine on breast cancer cell invasion was analyzed using a Matrigel assay. LRRC3B specific small interfering (si)RNA was constructed and transfected into breast cancer cells using Lipofectamine ® 2000 reagent. The influence of bupivacaine on LRRC3B expression was measured based on RT-qPCR. Additionally, the effect of LRRC3B silencing on the invasion of breast cancer cells treated with bupivacaine was analyzed. Compared with the control, LRRC3B expression significantly increased in MDA-MB-231 and in MCF-7 cells as the length of time increased (P<0.05), but the expression of the gene significantly declined in 2 types of cancer cell when the cells were transfected with siRNA-LRRC3B plasma (P<0.05). The administration of 50 µg/ml bupivacaine promoted maximum breast cancer cell invasion, and suppressed LRRC3B mRNA expression in cells. However, when LRRC3B was silenced in cancer cells, 20 µg/ml bupivacaine significantly promoted cancer cell invasion, indicating that bupivacaine suppresses the expression of LRRC3B and promotes cell invasion. The present study suggested that LRRC3B serves a protective role in preventing bupivacaine-induced breast cancer recurrence and metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Kong

Zou

2017

Oncology Letters

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“…Ninety-six paired frozen gastric tumor tissues and normal adjacent tissues were collected from the Tissue Bank at Chungnam National University Hospital. All samples were obtained with informed consent, and their use was approved by the institutional review board (19).…”

Section: Methodsmentioning

confidence: 99%

Specific expression and methylation of SLIT1, SLIT2, SLIT3, and miR-218 in gastric cancer subtypes

Kim

Baek

et al. 2016

International Journal of Oncology

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Abstract. SLIT has been suggested as a key regulator of cancer development and a promising therapeutic target for cancer treatment. Herein, we analyzed expression and methylation of SLIT1/SLIT2/SLIT3 in 11 gastric cancer cell lines, 96 paired gastric tumors and adjacent normal gastric tissues, and 250 gastric cancers provided by The Cancer Genome Atlas. Methylation of SLIT1/SLIT2/SLIT3 was found both in early gastric cancers, and in advanced gastric cancers. Even normal gastric tissue showed increased methylation of SLIT1 and SLIT3 that correlated with patient age. Furthermore, epigenetic inactivation of SLIT occurred in a gastric cancer subtype-dependent manner. SLIT2 and SLIT3 expression was reduced in Epstein-Barr virus-positive and microsatellite instability subtypes, but increased in the genomically stable subtype. Expression of miR-218 correlated negatively with methylation of SLIT2 or SLIT3. These findings suggest that a molecular subtype-specific therapeutic strategy is needed for targeting SLITs and miR-218 in treatment of gastric cancer.

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“…Anchorage-independent colony formation on these cell lines was determined as described previously [29] , with some modifications. Briefly, the cells were harvested and washed, and a total of 3×10 3 cells were resuspended in RPMI Medium 1640 containing 0.3% agarose.…”

Section: Soft Agar Assaymentioning

confidence: 99%

Transformation of human liver L-O2 cells mediated by stable HBx transfection

Zhang

Cai

et al. 2009

Acta Pharmacol Sin

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Aim: To explore the mechanism of hepatocarcinogenesis associated with the hepatitis B virus X protein (HBx), we investigated the role of HBx in transformation using human liver L-O2 cells stably transfected with HBx as a model. Methods: Plasmids encoding HBx were stably transfected into immortalized human liver L-O2 cells and rodent fibroblast NIH/3T3 cells. The expression of alfa-fetoprotein (AFP), c-Myc, HBx, and survivin in the engineered cells was examined by Western blotting. The malignant phenotype of the cells was demonstrated by anchorage-independent colony formation and tumor formation in nude mice. RNA interference assays, Western blotting, luciferase reporter gene assays and flow cytometry analysis were performed. The number of centrosomes in the L-O2-X cells was determined by γ-tubulin immunostaining. The effect of HBx on the transcriptional activity of human telomerase reverse transcriptase (hTERT) and hTERT activity in L-O2-X cells and/or 3T3-X cells was detected by the luciferase reporter gene assay and telomerase repeat amplification protocol (TRAP). Results: Stable HBx transfection resulted in a malignant phenotype in the engineered cells in vivo and in vitro. Meanwhile, HBx was able to increase the transcription of the NF-κB, AP-1, and survivin genes and to upregulate the expression levels of c-Myc and survivin. Abnormal centrosome duplication and activated hTERT were responsible for the transformation. Conclusion: Stable HBx transfection leads to genomic instability of host cells, which is responsible for hepatocarcinogenesis; meanwhile, transactivation by the HBx protein contributes to the development of hepatocellular carcinoma (HCC). The L-O2-X cell line is an ideal model for investigating the mechanism of HBx-mediated transformation.

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LRRC3B, Encoding a Leucine-Rich Repeat-Containing Protein, Is a Putative Tumor Suppressor Gene in Gastric Cancer

Cited by 49 publications

References 43 publications

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Specific expression and methylation of SLIT1, SLIT2, SLIT3, and miR-218 in gastric cancer subtypes

Transformation of human liver L-O2 cells mediated by stable HBx transfection

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