Small proline-rich protein-1B is overexpressed in human oral squamous cell cancer stem-like cells and is related to their growth through activation of MAP kinase signal

Michifuri, Yoshitaka; Hirohashi, Yoshihiko; Torigoe, Toshihiko; Miyazaki, Akira; Fujino, Jyunki; Tamura, Yasuaki; Tsukahara, Tomohide; Kanaseki, Takayuki; Kobayashi, Jun’ichi; Sasaki, Takanori; Takahashi, Akiko; Nakamori, Kenji; Yamaguchi, Akira; Hiratsuka, Hiroyoshi; Sato, Noriyuki

doi:10.1016/j.bbrc.2013.08.021

Cited by 43 publications

(41 citation statements)

References 31 publications

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“…Thus, it appears that RASSF4 has the properties of a Ras death effector. Like the other RASSF family members, RASSF4 expression is down-regulated in some human tumors [110, 163–165] and loss of RASSF4 expression has been linked to the maintenance of oral squamous cell carcinoma stem cells, where RASSF4 plays a role in inhibiting MAP kinase signaling [166]. However, somewhat contradictory to this, RASSF4 may also have the potential to be oncogenic.…”

Section: Other Rassf Family Membersmentioning

confidence: 99%

“…One further mechanism by which RASSF6 may function as a tumor suppressor is to inhibit NF-κB activity [168, 175], a function that is again shared with RASSF2 [158]. RASSF6 may keep Ras proliferative signals in check by inhibiting MAP kinase signaling [55], a similar effect observed with RASSF4 [166]. Thus RASSF6 has a number of potentially overlapping functions with RASSF2 and RASSF4, which may be due, in part, to the relatively high similarity between the two proteins.…”

Section: Other Rassf Family Membersmentioning

confidence: 99%

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Ras signaling through RASSF proteins

Donninger

Schmidt

Mezzanotte

et al. 2016

Seminars in Cell & Developmental Biology

107

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There are six core RASSF family proteins that contain conserved Ras Association domains and may serve as Ras effectors. They lack intrinsic enzymatic activity and appear to function as scaffolding and localization molecules. While initially being associated with pro-apoptotic signaling pathways such as Bax and Hippo, it is now clear that they can also connect Ras to a surprisingly broad range of signaling pathways that control senescence, inflammation, autophagy, DNA repair, ubiquitination and protein acetylation. Moreover, they may be able to impact the activation status of pro-mitogenic Ras effector pathways, such as the Raf pathway. The frequent epigenetic inactivation of RASSF genes in human tumors disconnects Ras from pro-death signaling systems, enhancing Ras driven transformation and metastasis. The best characterized members are RASSF1A and RASSF5 (NORE1A).

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Section: Other Rassf Family Membersmentioning

confidence: 99%

Section: Other Rassf Family Membersmentioning

confidence: 99%

Ras signaling through RASSF proteins

Donninger

Schmidt

Mezzanotte

et al. 2016

Seminars in Cell & Developmental Biology

107

View full text Add to dashboard Cite

show abstract

“…Required for apoptosis and growth inhibition [8] Inhibits MST2 activity [93] Modulates the MAP kinase signal downstream of the Ras signal [77] K-Ras [8] ST1, MST2 [177] MST1 [75] Not available 5A (Nore1A) 1q32 47.1 kDa Suppresses tumour growth via apoptosis induction or cell cycle delay [7,82] Regulates microtubule formation [182] Induces degradation of HIPK1 oncoprotein [183] Required for the TNFa mediated apoptosis and full activation of MST1 [80] Ras, Carma1 [182,184] MST1 [43,177] MST2 [177] tubulin, Aurora A [182] Mdm2 [183] Itch [185] Yes [80] resistant to TNFa-induced apoptosis, fail to activate Mst1 in vivo 5C (Nore1B, RAPL) 1q32 30.4 kDa…”

Section: Kdamentioning

confidence: 99%

“…One of the proposed regulators might be p53 [8], since H1299 cells (but not MCF-7 cells) are defective for p53. It was also suggested that RASSF4 may suppress the MAP kinase signal by suppression of ERK phosphorylation [77] thus providing another possible mechanism for RASSF4-mediated tumor suppression. To date, no known RASSF4 knockout has been generated.…”

Section: Rassf4mentioning

confidence: 99%

RASSF tumor suppressor gene family: Biological functions and regulation

et al. 2014

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a b s t r a c tGenetic changes through allelic loss and nucleic acid or protein modifications are the main contributors to loss of function of tumor suppressor proteins. In particular, epigenetic silencing of genes by promoter hypermethylation is associated with increased tumor severity and poor survival. The RASSF (Ras association domain family) family of proteins consists of 10 members, many of which are tumor suppressor proteins that undergo loss of expression through promoter methylation in numerous types of cancers such as leukemia, melanoma, breast, prostate, neck, lung, brain, colorectal and kidney cancers. In addition to their tumor suppressor function, RASSF proteins act as scaffolding agents in microtubule stability, regulate mitotic cell division, modulate apoptosis, control cell migration and cell adhesion, and modulate NFjB activity and the duration of inflammation. The ubiquitous functions of these proteins highlight their importance in numerous physiological pathways. In this review, we will focus on the biological roles of the RASSF family members and their regulation.

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“…Aldehyde dehydrogenase 1 (ALDH1) activity is a cancer stem-like cells(CSCs)/cancer-initiating cells(CICs) marker of various cancers [9–13]. We thus investigated whether ALDH1 activity is applicable to isolate urothelial CSCs/CICs.…”

Section: Resultsmentioning

confidence: 99%

GRIK2 has a role in the maintenance of urothelial carcinoma stem-like cells, and its expression is associated with poorer prognosis

et al. 2017

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Cancer stem-like cells (CSCs)/cancer-initiating cells (CICs) are small sub-population of cancer cells that are endowed with higher tumor-initiating ability, self-renewal ability and differentiation ability. CSCs/CICs could be isolated as high aldehyde dehydrogenase 1 activity cells (ALDH1high) from various cancer samples. In this study, we isolated urothelial carcinoma CSCs/CICs as ALDHhigh cells and investigated the molecular aspects. ALDH1high cells showed greater sphere-forming ability and higher tumor-initiating ability in immune-deficient mice than those of ALDH1low cells, indicating that CSCs/CICs were enriched in ALDH1high cells. cDNA microarray analysis revealed that an ionotropic glutamate receptor glutamate receptor, ionotropic, kainate 2 (GRIK2) was expressed in ALDH1high cells at a higher level than that in ALDH1low cells. GRIK2 gene knockdown by siRNAs decreased the sphere-forming ability and invasion ability, whereas GRIK2 overexpression increased the sphere-forming ability, invasion ability and tumorigenicity, indicating that GRIK2 has a role in the maintenance of CSCs/CICs. Immunohistochemical staining revealed that higher levels of GRIK2 and ALDH1 expression were related to poorer prognosis in urinary tract carcinoma cases. The findings indicate that GRIK2 has a role in the maintenance of urothelial CSCs/CICs and that GRIK2 and ALDH1 can be prognosis prediction markers for urinary tract carcinomas.

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Small proline-rich protein-1B is overexpressed in human oral squamous cell cancer stem-like cells and is related to their growth through activation of MAP kinase signal

Cited by 43 publications

References 31 publications

Ras signaling through RASSF proteins

Ras signaling through RASSF proteins

RASSF tumor suppressor gene family: Biological functions and regulation

GRIK2 has a role in the maintenance of urothelial carcinoma stem-like cells, and its expression is associated with poorer prognosis

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