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Article: α-parvin controls chondrocyte column formation and regulates long bone development.

Yuan, Jifan / Guo, Ling / Wang, Jiaxin / Zhou, Zhongjun / Wu, Chuanyue

2023 Volume 11, Issue 1, Page(s) 46

Abstract: Endochondral ossification requires proper control of chondrocyte proliferation, differentiation, survival, and organization. Here we show that knockout of α-parvin, an integrin-associated focal adhesion protein, from murine limbs causes defects in ... ...

Abstract	Endochondral ossification requires proper control of chondrocyte proliferation, differentiation, survival, and organization. Here we show that knockout of α-parvin, an integrin-associated focal adhesion protein, from murine limbs causes defects in endochondral ossification and dwarfism. The mutant long bones were shorter but wider, and the growth plates became disorganized, especially in the proliferative zone. With two-photon time-lapse imaging of bone explant culture, we provide direct evidence showing that α-parvin regulates chondrocyte rotation, a process essential for chondrocytes to form columnar structure. Furthermore, loss of α-parvin increased binucleation, elevated cell death, and caused dilation of the resting zones of mature growth plates. Single-cell RNA-seq analyses revealed alterations of transcriptome in all three zones (i.e., resting, proliferative, and hypertrophic zones) of the growth plates. Our results demonstrate a crucial role of α-parvin in long bone development and shed light on the cellular mechanism through which α-parvin regulates the longitudinal growth of long bones.
MeSH term(s)	Animals ; Mice ; Bone Development/genetics ; Cell Death ; Chondrocytes ; Growth Plate ; Osteogenesis/genetics
Chemical Substances	Parva protein, mouse
Language	English
Publishing date	2023-08-22
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2803313-9
ISSN	2095-6231 ; 2095-4700
ISSN (online)	2095-6231
ISSN	2095-4700
DOI	10.1038/s41413-023-00284-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Mitochondrial dynamics links PINCH-1 signaling to proline metabolic reprogramming and tumor growth

Ling Guo / Chuanyue Wu

Cell Stress, Vol 5, Iss 2, Pp 23-

2020 Volume 25

Abstract: Proline metabolism is critical for cellular response to microenvironmental stress in living organisms across different kingdoms, ranging from bacteria, plants to animals. In bacteria and plants, proline is known to accrue in response to osmotic and other ...

Abstract	Proline metabolism is critical for cellular response to microenvironmental stress in living organisms across different kingdoms, ranging from bacteria, plants to animals. In bacteria and plants, proline is known to accrue in response to osmotic and other stresses. In higher organisms such as human, proline metabolism plays important roles in physiology as well as pathological processes including cancer. The importance of proline metabolism in physiology and diseases lies in the fact that the products of proline metabolism are intimately involved in essential cellular processes including protein synthesis, energy production and redox signaling. A surge of protein synthesis in fast proliferating cancer cells, for example, results in markedly increased demand for proline. Proline synthesis is frequently unable to meet the demand in fast proliferating cancer cells. The inadequacy of proline or “proline vulnerability” in cancer may provide an opportunity for therapeutic control of cancer progression. To this end, it is important to understand the signaling mechanism through which proline synthesis is regulated. In a recent study (Guo et al., Nat Commun 11(1):4913, doi:10.1038/s41467-020-18753-6), we have identified PINCH-1, a component of cell-extracellular matrix (ECM) adhesions, as an important regulator of proline synthesis and cancer progression.
Keywords	tumor growth ; fibrosis ; mitochondrial dynamics ; proline metabolism ; cell-extracellular matrix adhesion ; pinch-1 ; Medicine ; R ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	Shared Science Publishers OG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mitochondrial dynamics links PINCH-1 signaling to proline metabolic reprogramming and tumor growth.

Guo, Ling / Wu, Chuanyue

Cell stress

2020 Volume 5, Issue 2, Page(s) 23–25

Abstract	Proline metabolism is critical for cellular response to microenvironmental stress in living organisms across different kingdoms, ranging from bacteria, plants to animals. In bacteria and plants, proline is known to accrue in response to osmotic and other stresses. In higher organisms such as human, proline metabolism plays important roles in physiology as well as pathological processes including cancer. The importance of proline metabolism in physiology and diseases lies in the fact that the products of proline metabolism are intimately involved in essential cellular processes including protein synthesis, energy production and redox signaling. A surge of protein synthesis in fast proliferating cancer cells, for example, results in markedly increased demand for proline. Proline synthesis is frequently unable to meet the demand in fast proliferating cancer cells. The inadequacy of proline or "proline vulnerability" in cancer may provide an opportunity for therapeutic control of cancer progression. To this end, it is important to understand the signaling mechanism through which proline synthesis is regulated. In a recent study (Guo
Language	English
Publishing date	2020-12-10
Publishing country	Austria
Document type	Journal Article ; Comment
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2021.02.241
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Article: Mechano-regulation of proline metabolism and cancer progression by kindlin-2.

Guo, Ling / Wu, Chuanyue

Molecular & cellular oncology

2019 Volume 6, Issue 3, Page(s) 1596003

Abstract: Alterations of cell mechano-environment and metabolism are common features of malignant neoplasm. We recently showed that increased stiffness of extracellular matrix is intrinsically linked to up-regulation of proline synthesis through a mechano- ... ...

Abstract	Alterations of cell mechano-environment and metabolism are common features of malignant neoplasm. We recently showed that increased stiffness of extracellular matrix is intrinsically linked to up-regulation of proline synthesis through a mechano-responsive fermitin family homolog 2 (FERMT2, best known as kindlin-2) and pyrroline-5-carboxylate reductase 1(PYCR1) complex, which in turn promotes collagen matrix synthesis, cell proliferation, survival, and cancer progression.
Language	English
Publishing date	2019-04-12
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2019.1596003
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Article ; Online: PINCH-1 promotes Δ

Cui, Chunhong / Wang, Jiaxin / Guo, Ling / Wu, Chuanyue

Amino acids

2021 Volume 53, Issue 12, Page(s) 1875–1890

Abstract: Proline metabolic reprogramming is intimately involved in cancer progression. We recently identified a critical role of PINCH-1, a cell-extracellular matrix (ECM) adhesion protein whose expression is elevated in lung adenocarcinoma, in the promotion of ... ...

Abstract	Proline metabolic reprogramming is intimately involved in cancer progression. We recently identified a critical role of PINCH-1, a cell-extracellular matrix (ECM) adhesion protein whose expression is elevated in lung adenocarcinoma, in the promotion of proline biosynthesis, fibrosis and lung adenocarcinoma growth. How PINCH-1 promotes proline biosynthesis, however, was incompletely understood. In this study, we show that PINCH-1 promotes the expression of Δ
MeSH term(s)	A549 Cells ; Adaptor Proteins, Signal Transducing/metabolism ; Adenocarcinoma of Lung/metabolism ; Animals ; Cell Line, Tumor ; Cell Proliferation/physiology ; Down-Regulation/physiology ; Humans ; LIM Domain Proteins/metabolism ; Lung Neoplasms/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Transgenic ; Proline/metabolism ; RNA, Messenger/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; LIM Domain Proteins ; Lims1 protein, mouse ; Membrane Proteins ; RNA, Messenger ; Proline (9DLQ4CIU6V)
Language	English
Publishing date	2021-07-20
Publishing country	Austria
Document type	Journal Article
ZDB-ID	1121341-3
ISSN	1438-2199 ; 0939-4451
ISSN (online)	1438-2199
ISSN	0939-4451
DOI	10.1007/s00726-021-03050-3
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Article ; Online: How signaling pathways link extracellular mechano-environment to proline biosynthesis: A hypothesis: PINCH-1 and kindlin-2 sense mechanical signals from extracellular matrix and link them to proline biosynthesis.

Chen, Keng / Guo, Ling / Wu, Chuanyue

BioEssays : news and reviews in molecular, cellular and developmental biology

2021 Volume 43, Issue 9, Page(s) e2100116

Abstract: We propose a signaling pathway in which cell-extracellular matrix (ECM) adhesion components PINCH-1 and kindlin-2 sense mechanical signals from ECM and link them to proline biosynthesis, a vital metabolic pathway for macromolecule synthesis, redox ... ...

Abstract	We propose a signaling pathway in which cell-extracellular matrix (ECM) adhesion components PINCH-1 and kindlin-2 sense mechanical signals from ECM and link them to proline biosynthesis, a vital metabolic pathway for macromolecule synthesis, redox balance, and ECM remodeling. ECM stiffening promotes PINCH-1 expression via integrin signaling, which suppresses dynamin-related protein 1 (DRP1) expression and mitochondrial fission, resulting in increased kindlin-2 translocation into mitochondria and interaction with Δ
MeSH term(s)	Extracellular Matrix ; Mitochondrial Dynamics ; Proline ; Pyrroline Carboxylate Reductases/metabolism ; Signal Transduction
Chemical Substances	Proline (9DLQ4CIU6V) ; Pyrroline Carboxylate Reductases (EC 1.5.1.-)
Language	English
Publishing date	2021-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202100116
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Article ; Online: PINCH-1 promotes IGF-1 receptor expression and skin cancer progression through inhibition of the GRB10-NEDD4 complex.

Wang, Xiaoxiao / Wang, Rong / Jiang, Kun / Zhu, Maohua / Guo, Ling / Wu, Chuanyue

Theranostics

2022 Volume 12, Issue 6, Page(s) 2613–2630

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Animals ; Carcinogenesis/pathology ; Carcinogens/metabolism ; Cell Proliferation ; GRB10 Adaptor Protein/metabolism ; GRB10 Adaptor Protein/pharmacology ; Keratinocytes ; Mice ; Receptor, IGF Type 1/genetics ; Skin/pathology ; Skin Neoplasms/chemically induced ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Tetradecanoylphorbol Acetate/adverse effects ; Tetradecanoylphorbol Acetate/metabolism
Chemical Substances	Carcinogens ; Grb10 protein, mouse ; GRB10 Adaptor Protein (151441-47-3) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2022-02-28
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.70744
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Article ; Online: CLP36 promotes p53 deficient sarcoma progression through suppression of atrophin-1 interacting protein-4 (AIP-4)-dependent degradation of YAP1.

Lu, Yixuan / Mu, Yongxin / Chen, Ju / Guan, Xinyuan / Guo, Ling / Wu, Chuanyue

Theranostics

2022 Volume 12, Issue 11, Page(s) 5051–5068

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; LIM Domain Proteins/genetics ; Mice ; Nerve Tissue Proteins ; Sarcoma/genetics ; Soft Tissue Neoplasms ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	LIM Domain Proteins ; Nerve Tissue Proteins ; Transcription Factors ; Tumor Suppressor Protein p53 ; atrophin-1 ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-07-04
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.72365
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Article ; Online: A mechanoresponsive PINCH-1-Notch2 interaction regulates smooth muscle differentiation of human placental mesenchymal stem cells.

Su, Jie / Guo, Ling / Wu, Chuanyue

Stem cells (Dayton, Ohio)

2021 Volume 39, Issue 5, Page(s) 650–668

Abstract: Extracellular matrix (ECM) stiffness plays an important role in the decision making process of smooth muscle differentiation of mesenchymal stem cells (MSCs) but the underlying mechanisms are incompletely understood. Here we show that a signaling axis ... ...

Abstract	Extracellular matrix (ECM) stiffness plays an important role in the decision making process of smooth muscle differentiation of mesenchymal stem cells (MSCs) but the underlying mechanisms are incompletely understood. Here we show that a signaling axis consisting of PINCH-1 and Notch2 is critically involved in mediating the effect of ECM stiffness on smooth muscle differentiation of MSCs. Notch2 level is markedly increased in ECM stiffness-induced smooth muscle differentiation of human placental MSCs. Knockdown of Notch2 from human placental MSCs effectively inhibits ECM stiffness-induced smooth muscle differentiation, whereas overexpression of North intracellular domain (NICD2) is sufficient to drive human placental MSC differentiation toward smooth muscle cells. At the molecular level, Notch2 directly interacts with PINCH-1. The interaction of Notch2 with PINCH-1 is significantly increased in response to ECM stiffness favoring smooth muscle differentiation. Furthermore, depletion of PINCH-1 from human placental MSCs reduces Notch2 level and consequently suppresses ECM stiffness-induced smooth muscle differentiation. Re-expression of PINCH-1, but not that of a Notch2-binding defective PINCH-1 mutant, in PINCH-1 knockdown human placental MSCs restores smooth muscle differentiation. Finally, overexpression of NICD2 is sufficient to override PINCH-1 deficiency-induced defect in smooth muscle differentiation. Our results identify an ECM stiffness-responsive PINCH-1-Notch2 interaction that is critically involved in ECM stiffness-induced smooth muscle differentiation of human placental MSCs.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Cell Differentiation/genetics ; Extracellular Matrix/genetics ; Female ; Gene Expression Regulation, Developmental/genetics ; Humans ; LIM Domain Proteins/genetics ; Mechanotransduction, Cellular/genetics ; Membrane Proteins/genetics ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Muscle, Smooth/growth & development ; Muscle, Smooth/metabolism ; Placenta/cytology ; Placenta/metabolism ; Placentation/genetics ; Pregnancy ; Receptor, Notch2/genetics ; Signal Transduction/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; LIM Domain Proteins ; LIMS1 protein, human ; Membrane Proteins ; Receptor, Notch2
Language	English
Publishing date	2021-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1002/stem.3347
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Article: PINCH-1 promotes Δ1-pyrroline-5-carboxylate synthase expression and contributes to proline metabolic reprogramming in lung adenocarcinoma

Cui, Chunhong / Wang, Jiaxin / Guo, Ling / Wu, Chuanyue

Amino acids. 2021 Dec., v. 53, no. 12

2021

Abstract	Proline metabolic reprogramming is intimately involved in cancer progression. We recently identified a critical role of PINCH-1, a cell-extracellular matrix (ECM) adhesion protein whose expression is elevated in lung adenocarcinoma, in the promotion of proline biosynthesis, fibrosis and lung adenocarcinoma growth. How PINCH-1 promotes proline biosynthesis, however, was incompletely understood. In this study, we show that PINCH-1 promotes the expression of Δ¹-pyrroline-5-carboxylate synthase (P5CS), a key enzyme that links glutamate metabolism to proline biosynthesis. Depletion of PINCH-1 from lung adenocarcinoma cells reduced the protein but not mRNA level of P5CS, resulting in down-regulation of the cellular level of P5C and cell proliferation. Treatment of the cells with protease inhibitor leupeptin effectively reversed PINCH-1 deficiency-induced reduction of the P5CS level. At the molecular level, PINCH-1, through its LIM2 domain, physically associated with P5CS in lung adenocarcinoma cells. Re-expression of wild type PINCH-1, but not that of the PINCH-1 LIM2 deletion mutant, in PINCH-1 deficient lung adenocarcinoma cells restored P5CS expression, proline biosynthesis and cell proliferation. Finally, P5CS expression, like that of PINCH-1, is elevated in human and mouse lung adenocarcinoma. Using a mouse model of lung adenocarcinoma in which PINCH-1 is conditionally ablated, we show that knockout of PINCH-1 from lung adenocarcinoma effectively reduced the P5CS level in vivo. Our results reveal an important role of PINCH-1 in the promotion of P5CS expression, which likely contributes to proline metabolic reprogramming and consequently lung adenocarcinoma progression.
Keywords	adenocarcinoma ; adhesion ; biosynthesis ; cell proliferation ; enzymes ; fibrosis ; gene expression ; glutamic acid ; humans ; lungs ; mice ; mutants ; neoplasm progression ; proline ; proteinase inhibitors
Language	English
Dates of publication	2021-12
Size	p. 1875-1890.
Publishing place	Springer Vienna
Document type	Article
ZDB-ID	1121341-3
ISSN	1438-2199 ; 0939-4451
ISSN (online)	1438-2199
ISSN	0939-4451
DOI	10.1007/s00726-021-03050-3
Database	NAL-Catalogue (AGRICOLA)

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