ArticleHuman cell2021
RP11-462C24.1 suppresses proliferation and invasion of colorectal carcinoma cells by regulating HSP70 through PI3K/AKT signaling pathway.
Article in Human cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Interplay between lncRNAs and the PI3K/AKT signaling pathway in the progression of digestive system neoplasms (Review).International journal of molecular medicine · 2025Review
- Long Non-Coding RNAs in Colorectal Cancer: Navigating the Intersections of Immunity, Intercellular Communication, and Therapeutic Potential.Biomedicines · 2023Review
- Long non-coding RNAs and JAK/STAT signaling pathway regulation in colorectal cancer development.Frontiers in genetics · 2023Review
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is the third leading cause of cancer-related death around the world. In this study, we investigated the roles of LncRNA RP11-462C24.1 in CRC. The expressions of RP11-462C24.1 in CRC tissues and cells were measured. Then, the effects of RP11-462C24.1 on CRC proliferation, cell cycle, apoptosis, and invasion were evaluated both in vivo and in vitro; Last, the underlying mechanisms of concerning the signaling pathway regulated by RP11-462C24.1 was determined. From the results, we found that RP11-462C24.1 was significantly decreased in CRC tumor tissues and the CRC cell lines, which were most significant in SW480 and HT-29 cell lines; moreover, transient overexpression of RP11-462C24.1 suppressed the growth and migration while promoted apoptosis of SW480 and HT-29 cells, while knockdown of RP11-462C24.1 has shown the opposite effects; RP11-462C24.1 may also inhibit the growth of CRC tumors in xenograft mice models; additionally, 70 kD heat shock proteins (HSP70) has been identified as one of the most significantly deferentially expressed genes by RNA-seq, and we further confirmed that RP11-462C24.1 may affect the growth and metathesis of CRC cells via regulating HSP70 and PI3K/AKT signaling pathway. In summary, these results indicated that RP11-462C24 may function as a tumor suppressor in the development of CRC.
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Registered trials
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