Shengjun Ma
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Shengjun Ma has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
Fanhua Kong
Department of Thoracic Surgery Liao Cheng People's Hospital Liaocheng People's Republic of China
1 shared publicationHui Tian
Department of Thoracic Surgery Qi Lu Hospital Affiliated to Shandong University Jinan People's Republic of China
1 shared publicationLianfu Zhang
Department of Thoracic Surgery Fei Cheng Hospital Affiliated to Shandong First Medical University Taian People's Republic of China
1 shared publicationLili Zhao
Department of Presonnel Section The Affiliated Taian City Central Hospital of Qingdao University Taian People's Republic of China
1 shared publicationPeng Wang
Department of Thoracic Surgery The Affiliated Taian City Centeral Hospital of Qingdao University Taian People's Republic of China
1 shared publicationRunqi Zhang
Department of Thoracic Surgery The Affiliated Taian City Centeral Hospital of Qingdao University Taian People's Republic of China
1 shared publication
Latest Publications
- 16 October 2023
- Published by Wiley in Journal of Biochemical and Molecular Toxicology
- Vol. 38 (1) , e23557
Resveratrol augments paclitaxel sensitivity by modulating miR‐671‐5p/STOML2/PINK1/Parkin‐mediated autophagy signaling in A549 cell
Background: Paclitaxel (PTX) resistance has become a notable clinical concern of Non‐small cell lung cancer (NSCLC). Our study aim is to investigate the effects of Resveratrol (RES) on NSCLC cells that have developed resistance to PTX. The NSCLC cell line A549 was employed in this investigation to establish a PTX‐resistant NSCLC cell line, denoted as A549/PTX, and established tumor transplantaton model. The presence of miR‐671‐5p, Stomatin‐like protein 2 (STOML2), and mitophagy biomarkers was evaluated using quantitative teal‐time PCR (qRT‐PCR) and western blot, The assessment of cell proliferation and apoptosis was conducted through the utilisation of colony formation and flow cytometry assays. The investigation of mitochondrial autolysosomes was conducted using transmission electron microscopy (TEM). Our results showed that the application of RES therapy resulted in a substantial improvement in the sansitivity of A549/PTX cells. RES exhibited an augmentation of apoptosis and a suppression of mitophagy in A549/PTX cells. RES induced an upregulation in the expression of miR‐671‐5p. This, in turn, leaded to the inhibition of STOML2, a protein that directly interacts with PINK1. In summary, our research indicates that RES improved the susceptibility of A549/PTX cells to PTX through miR‐671‐5p‐mediated STOML2 inhibition.
- 16 October 2023
- Published by Wiley in Journal of Biochemical and Molecular Toxicology
- Vol. 38 (1) , e23557
Resveratrol augments paclitaxel sensitivity by modulating miR‐671‐5p/STOML2/PINK1/Parkin‐mediated autophagy signaling in A549 cell
Background: Paclitaxel (PTX) resistance has become a notable clinical concern of Non‐small cell lung cancer (NSCLC). Our study aim is to investigate the effects of Resveratrol (RES) on NSCLC cells that have developed resistance to PTX. The NSCLC cell line A549 was employed in this investigation to establish a PTX‐resistant NSCLC cell line, denoted as A549/PTX, and established tumor transplantaton model. The presence of miR‐671‐5p, Stomatin‐like protein 2 (STOML2), and mitophagy biomarkers was evaluated using quantitative teal‐time PCR (qRT‐PCR) and western blot, The assessment of cell proliferation and apoptosis was conducted through the utilisation of colony formation and flow cytometry assays. The investigation of mitochondrial autolysosomes was conducted using transmission electron microscopy (TEM). Our results showed that the application of RES therapy resulted in a substantial improvement in the sansitivity of A549/PTX cells. RES exhibited an augmentation of apoptosis and a suppression of mitophagy in A549/PTX cells. RES induced an upregulation in the expression of miR‐671‐5p. This, in turn, leaded to the inhibition of STOML2, a protein that directly interacts with PINK1. In summary, our research indicates that RES improved the susceptibility of A549/PTX cells to PTX through miR‐671‐5p‐mediated STOML2 inhibition.