m7GライターのMETTL1とBUD23の過剰発現は,腎臓のクリア細胞癌において腫瘍性をもたらす
Anni Su1,2, Jessica Tieng1,2, Xueying S Xu2
1Epigenetics and RNA Biology Laboratory, Charles Perkins Centre, University of Sydney, Camperdown, Australia.
The Journal of pathology
|August 29, 2025
まとめ
N7-メチルグアノシン (m7G) レーターであるMETTL1とBUD23は腎臓がんで過剰発現し,腫瘍の成長を誘導する. これらのm7Gライターをターゲットにすることで,腎臓のクリア細胞癌 (KIRC) の新しい治療戦略を提供することができる.
科学分野:
- 腫瘍学
- 分子生物学
- エピジェネティクス
背景:
- N7-メチルグアノシン (m7G) 改変は,様々な癌に関与しています.
- 腎臓のクリア細胞癌 (KIRC) に関する m7Gライターの特定の役割はよく理解されていません.
研究 の 目的:
- KIRCにおけるm7Gライター,特にMETTL1とBUD23の役割を調査する.
- KIRCにおける予後バイオマーカーおよび治療標的としての可能性を評価する.
主な方法:
- KIRC患者のサンプルにおけるMETTL1とBUD23発現の分析
- KIRC細胞系におけるMETTL1またはBUD23のノックダウンを含む機能研究.
- 腫瘍抑制遺伝子mRNAにおけるm7G変異の調査.
主要な成果:
- METTL1とBUD23は高度なKIRCで過剰発現し,生存率の低下と相関しています.
- METTL1またはBUD23のノックダウンは,KIRC細胞の増殖,コロニー形成,および移動を抑制する.
- METTL1とBUD23の発現は,METTL1媒介のm7G変異の証拠で,腫瘍抑制遺伝子発現と逆相関しています.
結論:
- METTL1とBUD23は,KIRCにおいて腫瘍性作用を有する.
- これらのm7Gライターは,KIRC治療の潜在的予後バイオマーカーであり,治療目標である.
関連する概念動画
mTOR Signaling and Cancer Progression
3.9K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
3.9K
Abnormal Proliferation
4.6K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.6K
Induced Pluripotent Stem Cells
4.4K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
Somatic...
4.4K
Master Transcription Regulators
7.0K
Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
7.0K
PI3K/mTOR/AKT Signaling Pathway
3.9K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.9K
Metastasis
5.7K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.7K


