Related Experiment Video

Updated: Sep 6, 2025

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

253

IFI35 Promotes Renal Cancer Progression by Inhibiting pSTAT1/pSTAT6-Dependent Autophagy

Dafei Chai1,2,3,4, Shang Yuchen Shi5, Navid Sobhani4

  • 1Cancer Institute, Xuzhou Medical University, Xuzhou 221002, China.

Cancers
|June 24, 2022
PubMed

Insights

Interferon-induced protein 35 (IFI35) is elevated in renal cell cancer (RCC), promoting tumor growth. Reducing IFI35 inhibits RCC progression by activating autophagy via the pSTAT1/pSTAT6 pathway, suggesting IFI35 as a therapeutic target.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Interferon-induced protein 35 (IFI35) regulates antiviral immune responses.
  • The role of IFI35 in renal cell cancer (RCC) pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the expression, function, and therapeutic potential of IFI35 in RCC.
  • To elucidate the molecular mechanisms underlying IFI35's role in RCC progression.

Main Methods:

  • Analysis of IFI35 expression in RCC tissues and cell lines.
  • In vitro and in vivo studies involving IFI35 knockdown in RCC models.
  • Investigation of autophagy induction and STAT1/STAT6 signaling pathways.

Main Results:

  • IFI35 expression is significantly upregulated in RCC tissues and correlates with poor prognosis.
  • IFI35 knockdown suppresses RCC cell proliferation, migration, and metastasis in vitro and in vivo.
  • IFI35 knockdown induces autophagy via enhanced expression of autophagy-related genes (LC3-II, Beclin-1, ATG-5).
  • The tumor-suppressive effects of IFI35 knockdown are mediated by pSTAT1/pSTAT6-dependent autophagy.

Conclusions:

  • IFI35 promotes RCC progression through pSTAT1/pSTAT6-dependent autophagy.
  • IFI35 represents a potential diagnostic biomarker and therapeutic target for renal cell cancer.
Keywords:
IFI35RCCautophagydiagnostic biomarkerrenal cancertherapeutic target

More Related Videos

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma13:18

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

Published on: March 3, 2023

1.3K
Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells09:51

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells

Published on: June 30, 2023

1.0K

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
3.9K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.2K
Abnormal Proliferation02:23

Abnormal Proliferation

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
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.2K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.4K