Inactivation of Rab23 inhibits the invasion and motility of pancreatic duct adenocarcinoma

Cai, Zhenzhai; Xu, Lixiang; Cai, J.L.; Wang, J.S.; Zhou, Bin; Hu, Hao

doi:10.4238/2015.march.30.31

Cited by 11 publications

(5 citation statements)

References 26 publications

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“…Survival analysis indicated that Rab23 was positively associated with the poor OS and DFS rates of OC patients. This is consistent with the studies by Cai et al (10) on pancreatic duct adenocarcinoma, and by Chang et al (11) on prostate cancer. However, the results are conflicting with studies in thyroid and breast cancer (8,9).…”

Section: Discussionsupporting

confidence: 82%

“…In recent years, tumor-promoting roles for Rab23 have been reported in several types of tumors. In 2015, Cai et al (10) reported that Rab23 activated the invasion and motility of pancreatic duct adenocarcinoma cells. In 2017, Chang et al (11) reported that the downregulation of Rab23 in prostate cancer could inhibit tumor growth in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

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Rab23 promotes the cisplatin resistance of ovarian cancer via the Shh-Gli-ABCG2 signaling pathway

Zhang

Feng²,

Wang

et al. 2018

Oncol Lett

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Abstract.As a novel member of the Rab GTPase family, the role of Rab23 has been reported in multiple types of tumor. However, to the best of our knowledge, the role of Rab23 in ovarian cancer (OC) has not yet been reported. In the present study, immunohistochemistry analysis demonstrated that Rab23 was upregulated in OC tissue; survival analysis indicated that Rab23 expression was associated with a reduced overall survival (OS) rate and disease-free survival (DFS) time. In vitro experiments also demonstrated the increased expression of Rab23 in the OC cells lines, A2780 and SKOV-3, compared with in the normal ovarian cell line, IOSE80. Following the silencing of ABCG2 in SKOV-3 cells, ATP-binding cassette sub-family G member 2 (ABCG2) expression was significantly downregulated both at the RNA and protein levels. The cisplatin (DDP) IC 50 declined from 43.09±7.12 µmol/l in control cells to 26.46±5.38 µmol/l in SKOV-3 cells with silenced Rab23. In contrast, in A2780 cells overexpressing Rab23 (A2780-Rab23), ABCG2 expression was significantly upregulated and the DDP IC 50 increased from 27.42±6.54 µmol/l in control cells to 45.92±5.23 µmol/l in A2780-Rab23. Investigation into the potential molecular mechanisms for this revealed that the expression of sonic hedgehog (Shh) and Gli family zinc finger 1 (Gli1) was increased in A2780-Rab23 cells, whereas silencing Rab23 in SKOV-3 cells significantly inhibited the expression of Shh and Gli1. The Gli1 inhibitor GANT-61 significantly abrogated the increased ABCG2 expression in A2780-Rab23 cells. Furthermore, the DDP IC 50 in A2780-Rab23 cells decreased significantly following the silencing of ABCG2 expression; the IC 50 declined from 51.66±8.32 µmol/l in A2780-Rab23 cells to 25.61±6.17 µmol/l in A2780-Rab23 cells with silenced ABCG2. Collectively, the results indicate that Rab23 promotes the DDP resistance of OC cells via the Shh-Gli1-ABCG2 pathway, providing the proof of principle for the further investigation of drug resistance therapy targeting Rab23.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Rab23 promotes the cisplatin resistance of ovarian cancer via the Shh-Gli-ABCG2 signaling pathway

Zhang

Feng²,

Wang

et al. 2018

Oncol Lett

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“…RAB23 is a member of the Rab family of the GTPases and is a negative regulator of the Sonic hedgehog signaling pathway . It plays important roles in the development of cancer . For example, Liu et al showed that RAB23 expression was upregulated in breast cancer, and overexpression of RAB23 suppressed breast cancer cell growth and proliferation and induced cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…[31][32][33] It plays important roles in the development of cancer. [34][35][36][37] For example, Liu et al 38 showed that RAB23 expression was upregulated in breast cancer, and overexpression of RAB23 suppressed breast cancer cell growth and proliferation and induced cell apoptosis. Jiang et al 39 demonstrated that RAB23 was overexpressed in bladder cancer tissues, and the higher expression of RAB23 was associated with tumor invasion depth.…”

Section: Discussionmentioning

confidence: 99%

miR‐384 suppressed renal cell carcinoma cell proliferation and migration through targeting RAB23

Liu

Feng

et al. 2018

J of Cellular Biochemistry

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microRNAs (miRNAs) are noncoding, short, and endogenous RNAs that play crucial roles in tumor progression at the post‐transcriptional level. Here, we studied the role of miR‐384 in the pathogenesis of renal cell carcinoma (RCC). We demonstrated that miR‐384 expression was downregulated in the RCC specimens compared with nontumor specimens. Moreover, we showed that RAB23 expression was upregulated in the RCC tissues compared with nontumor tissues. Furthermore, we demonstrated that low expression of miR‐384 was correlated with high levels of RAB23 in RCC tissues. We also demonstrated that the RAB23 was a direct target gene of miR‐384 in RCC cells. In addition, overexpression of miR‐384 suppressed RCC cell proliferation, cell cycle, and cell migration. Furthermore, ectopic expression of RAB23 promoted RCC cell proliferation, cell cycle, and cell migration. These data suggested that miR‐384 played a tumor suppressor microRNA in the development of RCC partly through inhibiting RAB23 expression.

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“…Also altered expression of Rab23 has been reported in different types of cancers [163,164,165,166,167]. In more detail, its overexpression promotes cell migration and invasion through modulation of Rac1 activity, as well as cell proliferation [163,164,165,167]. Rab23 localizes to the plasma membrane and the endocytic pathway [173], however not much is known about its role in membrane traffic regulation.…”

Section: Rab Proteins In Cancermentioning

confidence: 99%

Rab GTPases: Switching to Human Diseases

Guadagno

Progida

2019

Cells

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Rab proteins compose the largest family of small GTPases and control the different steps of intracellular membrane traffic. More recently, they have been shown to also regulate cell signaling, division, survival, and migration. The regulation of these processes generally occurs through recruitment of effectors and regulatory proteins, which control the association of Rab proteins to membranes and their activation state. Alterations in Rab proteins and their effectors are associated with multiple human diseases, including neurodegeneration, cancer, and infections. This review provides an overview of how the dysregulation of Rab-mediated functions and membrane trafficking contributes to these disorders. Understanding the altered dynamics of Rabs and intracellular transport defects might thus shed new light on potential therapeutic strategies.

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Inactivation of Rab23 inhibits the invasion and motility of pancreatic duct adenocarcinoma

Cited by 11 publications

References 26 publications

Rab23 promotes the cisplatin resistance of ovarian cancer via the Shh-Gli-ABCG2 signaling pathway

Rab23 promotes the cisplatin resistance of ovarian cancer via the Shh-Gli-ABCG2 signaling pathway

miR‐384 suppressed renal cell carcinoma cell proliferation and migration through targeting RAB23

Rab GTPases: Switching to Human Diseases

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