LASP1 (internal region)
- Known as:
- LASP1 (middlesequence region)
- Catalog number:
- Y213819
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- LASP1 (internal region)
Related genes to: LASP1 (internal region)
- Gene:
- LASP1 NIH gene
- Name:
- LIM and SH3 protein 1
- Previous symbol:
- -
- Synonyms:
- MLN50, Lasp-1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2016-10-05
Related products to: LASP1 (internal region)
Related articles to: LASP1 (internal region)
- Following the publication of the above article, an interested reader drew to the authors' attention that, for the cell invasion assay experiments shown in Fig. 2D on p. 5, there appeared to be an overlapping section of data comparing between the Sao‑2/Control and MG‑63/siH19 panels, such that these data had been derived from the same original source where the panels were intended to portray the results from differently performed epxeriments. Upon examining their original data, the authors have realized that, in Fig. 2D, an inadvertent error was made in the copying and pasting of the two groups of pictures, resulting in the image belonging to the Saos‑2 cell experiment being mistakenly pasted as the image for the MG‑63 cell experiment. The authors carefully checked the original pictures and the experimental record, and found that the two groups of cells were close to the same morphology. The corrected version of Fig. 2, containing data from an alternatively performed experiment for Fig. 2D, is shown on the next page. Note that the error did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Oncology Reports 46: 207, 2021; DOI: 10.3892/or.2021.8158]. - Source: PubMed
Publication date: 2024/04/19
Jin HaoWang HuanJin XinWang Wenbo - Glutamate dehydrogenase 1 (GLUD1) is implicated in oncogenesis. However, little is known about the relationship between GLUD1 and hepatocellular carcinoma (HCC). In the present study, we demonstrated that the expression levels of GLUD1 significantly decreased in tumors, which was relevant to the poor prognosis of HCC. Functionally, GLUD1 silencing enhanced the growth and migration of HCC cells. Mechanistically, the upregulation of interleukin-32 through AKT activation contributes to GLUD1 silencing-facilitated hepatocarcinogenesis. The interaction between GLUD1 and AKT, as well as α-ketoglutarate regulated by GLUD1, can suppress AKT activation. In addition, LIM and SH3 protein 1 (LASP1) interacts with GLUD1 and induces GLUD1 degradation via the ubiquitin-proteasome pathway, which relies on the E3 ubiquitin ligase synoviolin (SYVN1), whose interaction with GLUD1 is enhanced by LASP1. In hepatitis B virus (HBV)-related HCC, the HBV X protein (HBX) can suppress GLUD1 with the participation of LASP1 and SYVN1. Collectively, our data suggest that GLUD1 silencing is significantly associated with HCC development, and LASP1 and SYVN1 mediate the inhibition of GLUD1 in HCC, especially in HBV-related tumors. - Source: PubMed
Publication date: 2024/04/08
You Hong-JuanLi QiMa Li-HongWang XingZhang Huan-YangWang Yu-XinBao En-SiZhong Yu-JieKong De-LongLiu Xiang-YeKong Fan-YunZheng Kui-YangTang Ren-Xian - - Source: PubMed
Publication date: 2024/02/19
Beckmann DeniseKrause AnnikaHansen UweKiener Hans PKaronitsch ThomasBlüml StephanKremerskothen JoachimPavenstädt HermannPap ThomasKorb-Pap Adelheid - Human papillomaviruses (HPV) are a major cause of malignancy, contributing to ∼5% of all human cancers worldwide, including most cervical cancer cases and a growing number of ano-genital and oral cancers. The major HPV viral oncogenes, E6 and E7, manipulate many host cellular pathways that promote cell proliferation and survival, predisposing infected cells to malignant transformation. Despite the availability of highly effective vaccines, there are still no specific anti-viral therapies targeting HPV or treatments for HPV-associated cancers. As such, a better understanding of viral-host interactions may allow the identification of novel therapeutic targets. Here, we demonstrate that the actin-binding protein LASP1 is upregulated in cervical cancer and significantly correlates with a poorer overall survival. In HPV positive cervical cancer, LASP1 depletion significantly inhibited proliferation , whilst having minimal effects in HPV negative cervical cancer cells. Furthermore, we show that the LASP1 SH3 domain is essential for LASP1-mediated proliferation in these cells. Mechanistically, we show that HPV E7 regulates LASP1 at the post-transcriptional level by repressing the expression of miR-203, which negatively regulated mRNA levels by binding to its 3'UTR. Finally, we demonstrated that LASP1 expression is required for the growth of HPV positive cervical cancer cells in an tumourigenicity model. Together, these data demonstrate that HPV induces LASP1 expression to promote proliferation and survival role in cervical cancer, thus identifying a potential therapeutic target in these cancers. - Source: PubMed
Publication date: 2024/01/15
Patterson Molly RMeijers Aniek SRyder Emma LScarth James AEvans DebraTurner Amy LWasson Christopher WDarell Janne ETheobald DaisyCogan JosephJames Claire DWang MiaoLadbury John EMorgan Iain MSamson AdelMorgan Ethan LMacdonald Andrew - Astragaloside IV (AS-IV) has exhibited pivotal anti-cancer efficacy in multiple types of cancer, including colorectal cancer (CRC). Meanwhile, circular RNA (circRNA) circ_0001615 has been reported to be involved in the malignant development of CRC. Herein, this study is expected to figure out the interaction between circ_0001615 and AS-IV on CRC progression. The 50% inhibition concentration (IC50), proliferation, apoptosis, and migration were detected by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and wound healing assays. The expression of related proteins was examined by western blot. Circ_0001615, microRNA-873-5p (miR-873-5p), and LIM and SH3 protein 1 (LASP1) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The binding between miR-873-5p and circ_0001615, or LASP1, was predicted by Starbase, followed by verification by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The biological role of circ_0001615 and AS-IV on CRC tumor growth was detected by the xenograft tumor model in vivo. According to the IC50 of AS-IV in CRC cells, the 100 ng/mL AS-IV treatment for 24 h was chosen for the following research: Our data confirmed that AS-IV is a beneficial anti-cancer agent in CRC cells. Furthermore, circ_0001615 and LASP1 expression were increased, and miR-873-5p was decreased in CRC patients and cell lines, whereas their expression exhibited an opposite trend in AS-IV-treated cells. Functionally, applying AS-IV might act as a beneficial anti-cancer effect by downregulating circ_0001615 in CRC cells in vitro. Mechanically, circ_0001615 serves as a sponge for miR-873-5p to affect LASP1 expression. In addition, AS-IV inhibited CRC cell growth in vivo by modulating circ_0001615. Overall, AS-IV could mitigate CRC development, at least in part, through the circ_0001615/miR-873-5p/LASP1 axis. These findings support a theoretical basis for an in-depth study of the function of AS-IV and the clinical treatment of CRC. - Source: PubMed
Kong PengfeiTang XuemeiLiu FangTang Xuegui