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ACHARIYA ARTS AND SCIENCE COLLEGE
(AFFILATED TO PONDICHERRY UNIVERSITY)

DEPARTMENTAL SEMINAR
BIOTECHNOLOGY DEPARTMENT
Topic:-Molecular Mechanism Of Cancer Metastasis

Presentation by
Gopi Krishna Giri
Overview
What is metastasis?
Molecular mechanisms of metastasis
Signalling pathways involved in
metastasis

2
I) What is cancer metastasis?
Cancer defines as a population of cells that
have lost their normal controls of growth and
differentiation and are proliferating without
check.
Metastasis is the process by which a tumor
cell leaves the primary tumor, travels to a
distant site via the circulatory system, and
establishes a secondary tumor.
3
Forms of cancer metastasis

4

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Cellular and molecular basis pathogenesis of cancer
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This document discusses neoplasia and cancer. It defines a neoplasm as abnormal tissue growth that exceeds normal limits. Cancer is the term for malignant tumors. The molecular basis of cancer involves genetic damage to proto-oncogenes, tumor suppressor genes, apoptosis genes, and DNA repair genes. Essential alterations for cancer include self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, defects in DNA repair, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize. Cancer development is a multistep process involving genetic alterations that affect cell cycle regulation, growth signals, tumor suppressor pathways, apoptosis, and DNA repair.

Preferential metastatic sites
Primary tumour

Common distant site (s)

Breast’ adenocarcinoma

Bone, brain, adrenal

Prostate adenocarcinoma

Bone

Lung small cell carcinoma

Bone, brain, liver

Skin cutaneous melanoma

Brain, liver, Bowel

Thyroid adenocarcinoma

Bone

Kidney clear cell carcinoma

Bone, liver, thyroid

Testis carcinoma

Liver

Bladder carcinoma

Brain

Neuroblastoma

Liver, adrenal
5
Reason for organ selectivity
Mechanistic theory: determined by the
pattern of blood flow.
“Seed and soil” theory: the provision of a
fertile environment in which compatible
tumor cells could grow

6
Determining factors
Appropriate growth factors or
extracellular matrix environment
Compatible adhesion sites on the
endothelial lumenal surface
Selective chemotaxis at which the organ
producing some soluble attraction factors
to the tumor cells
7
II) Molecular mechanisms of
metastasis

8

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1) Cancer begins as abnormal cells that grow uncontrollably and can become invasive, spreading to other parts of the body. 2) There are several types of cancer including carcinomas, sarcomas, leukemias, lymphomas, and central nervous system cancers. 3) Metastasis is when cancer cells spread from the original tumor site through the bloodstream or lymphatic system and form new tumors in other parts of the body. The major steps in metastasis include invasion, circulation, arrest in distant organs, and growth of new tumors.

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Cancer is caused by uncontrolled cell growth and can spread through invasion and metastasis. There are over 200 types of cancer that can affect different parts of the body. The cellular basis of cancer involves a disruption of the normal balance between new cell growth and cell death. Cancer arises due to mutations in genes controlling cell proliferation, which can be caused by carcinogens, radiation, viruses, or heredity. Oncogenes promote cancer by stimulating cell growth and division, while tumor suppressor genes normally inhibit cell proliferation, and inactivation of both copies allows for uncontrolled growth.

5 major steps in metastasis
1.

2.
3.
4.
5.

Invasion and infiltration of surrounding normal host
tissue with penetration of small lymphatic or
vascular channels;
Release of neoplastic cells, either or single cells or
small clumps, into the circulation;
Survival in the circulation;
Arrest in the capillary beds of distant organs;
Penetration of the lymphatic or blood vessel walls
followed by growth of the disseminated tumor cells
9
10
Stages of metastasis
Invasion : primary tumour cells enter
circulation
Circulation to the secondary site of tumour
growth
Colonisation : formation of secondary
tumour

11
Tumor invasion
1. Translocation of cells across extracellular

matrix barriers
2. Lysis of matrix protein by specific

proteinases
3. Cell migration
12

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This document discusses cancer invasion and metastasis. It begins by introducing the concepts of invasion and metastasis, where cancer spreads from the primary site to distant tissues. It then discusses the somatic evolution of cancer and the multiple genetic alterations required for malignancy. The document covers clinical and pathological correlations with metastasis risk, and the "seed and soil" hypothesis of why cancers metastasize to certain organs. It outlines the basic steps in the metastatic cascade, including invasion, intravasation, arrest and extravasation at distant sites. Finally, it discusses the implications of the traditional progression model, including the rarity of metastatic cells and prevention of metastasis through early detection and treatment.

Components of invasion
a) Matrix degrading enzymes
b) Cell adhesion
c) Cell motility

13
a) Matrix degrading enzymes
Required for a controlled degradation of
components of the extracellular matrix
(ECM)
The proteases involved in this process are
classified into serine-, cysteine-, aspartyl-,
and metalloproteinase.
14
MMP family

15
Matrix metalloproteinases (MMP)
16 members, subdivided into 4 groups,
based on their structural characteristics and
substrate specificities
Soluble and secreted groups; collagenase,
gelatinase and stromelysins
Membrane type (MT-MMP) group are
anchored in the plasma membrane
A zinc ion in the active centre of the
protease is required for their catalytic
activities.
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Tumor growth requires angiogenesis to develop new blood vessels. This process is regulated by a balance of pro-angiogenic and anti-angiogenic factors. Tumors disrupt this balance by inducing hypoxia and secreting factors like VEGF, which activate the "angiogenic switch" and promote new vessel growth. This allows tumors to recruit blood vessels to supply nutrients and remove waste. Anti-angiogenic therapies aim to block this process by targeting VEGF and its receptors. Drugs like bevacizumab and sorafenib inhibit angiogenesis to limit tumor growth and progression.

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Regulation of MMP
MMP is controlled by an increased expression on a
transcriptional level.
MMPs are calcium-dependent proteases, which are
synthesized as a inactive proenzymes and are
activated by the cleavage of a propeptide.
MMP activity is regulated by specific inhibitors, the
tissue inhibitors of MMP (TIMPs). Binding TIMP to
MMP is in a 1:1 stoichiometry.
MMP2 and MMP9, which cleave type IV collagen
the major constituent of basement membrane, are
believed to be of special importance
17
Serine proteases
Serine protease involved in ECM degradation are
plasmin, plasminogen activators and cathepsin G.
Plasmin is believed to be the most important
serine protease, firstly because its ability to
degrade several matrix components like gelatin,
fibronectin or laminin, and secondly by the
possible activation of numerous proforms of MMPs
by propeptide cleavage.
Plasmin is synthesized in its inactive proform,
plasminogen, which can be converted to plasmin
by plasminogen activator.
18
Plasminogen activator
Two main types : urokinase (uPA) and
tissue (tPA).
uPA is bound to the surface of tumor cells
by means of a specific receptor (uPAR)
There are specific inhibitors (PAI-1 and
PAI-2) for the PA.

19
Interaction between tumour cells
and the surrounding connective
tissue

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Cell adhesion and metastasis

21
b) Cell attachment
1. Integrin: cell-matrix adhesion
2. E- cadherin/catenin adhesion complex:

cell-cell adhesion

22
1) Integrin
Heterodimeric transmembrane receptors
consists of α and β subunits
Function to provide interactions between
cells and macromolecules in the ECM
Integrin can affect the transcription of
MMP genes

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Integrin signaling

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2) E- cadherin and catenin
complex
Most important cell-cell adhesion
molecules
Reduce expression of E-cadherin and
catenin increase the invasiveness of
tumor cells

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Cadherin-mediated cell-cell
adhesion

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p120 catenin

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Small Rho GTPase
Stimuli

Cdc42

Rac1
GTP

GTP

Pak1

MLC Kinase

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Stress fibers

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Insulin-like growth factor II
Autotaxin

37
HGF/scatting factor
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Molecular mechanism of cancer metastasis

  • 1. ACHARIYA ARTS AND SCIENCE COLLEGE (AFFILATED TO PONDICHERRY UNIVERSITY) DEPARTMENTAL SEMINAR BIOTECHNOLOGY DEPARTMENT Topic:-Molecular Mechanism Of Cancer Metastasis Presentation by Gopi Krishna Giri
  • 2. Overview What is metastasis? Molecular mechanisms of metastasis Signalling pathways involved in metastasis 2
  • 3. I) What is cancer metastasis? Cancer defines as a population of cells that have lost their normal controls of growth and differentiation and are proliferating without check. Metastasis is the process by which a tumor cell leaves the primary tumor, travels to a distant site via the circulatory system, and establishes a secondary tumor. 3
  • 4. Forms of cancer metastasis 4
  • 5. Preferential metastatic sites Primary tumour Common distant site (s) Breast’ adenocarcinoma Bone, brain, adrenal Prostate adenocarcinoma Bone Lung small cell carcinoma Bone, brain, liver Skin cutaneous melanoma Brain, liver, Bowel Thyroid adenocarcinoma Bone Kidney clear cell carcinoma Bone, liver, thyroid Testis carcinoma Liver Bladder carcinoma Brain Neuroblastoma Liver, adrenal 5
  • 6. Reason for organ selectivity Mechanistic theory: determined by the pattern of blood flow. “Seed and soil” theory: the provision of a fertile environment in which compatible tumor cells could grow 6
  • 7. Determining factors Appropriate growth factors or extracellular matrix environment Compatible adhesion sites on the endothelial lumenal surface Selective chemotaxis at which the organ producing some soluble attraction factors to the tumor cells 7
  • 8. II) Molecular mechanisms of metastasis 8
  • 9. 5 major steps in metastasis 1. 2. 3. 4. 5. Invasion and infiltration of surrounding normal host tissue with penetration of small lymphatic or vascular channels; Release of neoplastic cells, either or single cells or small clumps, into the circulation; Survival in the circulation; Arrest in the capillary beds of distant organs; Penetration of the lymphatic or blood vessel walls followed by growth of the disseminated tumor cells 9
  • 10. 10
  • 11. Stages of metastasis Invasion : primary tumour cells enter circulation Circulation to the secondary site of tumour growth Colonisation : formation of secondary tumour 11
  • 12. Tumor invasion 1. Translocation of cells across extracellular matrix barriers 2. Lysis of matrix protein by specific proteinases 3. Cell migration 12
  • 13. Components of invasion a) Matrix degrading enzymes b) Cell adhesion c) Cell motility 13
  • 14. a) Matrix degrading enzymes Required for a controlled degradation of components of the extracellular matrix (ECM) The proteases involved in this process are classified into serine-, cysteine-, aspartyl-, and metalloproteinase. 14
  • 16. Matrix metalloproteinases (MMP) 16 members, subdivided into 4 groups, based on their structural characteristics and substrate specificities Soluble and secreted groups; collagenase, gelatinase and stromelysins Membrane type (MT-MMP) group are anchored in the plasma membrane A zinc ion in the active centre of the protease is required for their catalytic activities. 16
  • 17. Regulation of MMP MMP is controlled by an increased expression on a transcriptional level. MMPs are calcium-dependent proteases, which are synthesized as a inactive proenzymes and are activated by the cleavage of a propeptide. MMP activity is regulated by specific inhibitors, the tissue inhibitors of MMP (TIMPs). Binding TIMP to MMP is in a 1:1 stoichiometry. MMP2 and MMP9, which cleave type IV collagen the major constituent of basement membrane, are believed to be of special importance 17
  • 18. Serine proteases Serine protease involved in ECM degradation are plasmin, plasminogen activators and cathepsin G. Plasmin is believed to be the most important serine protease, firstly because its ability to degrade several matrix components like gelatin, fibronectin or laminin, and secondly by the possible activation of numerous proforms of MMPs by propeptide cleavage. Plasmin is synthesized in its inactive proform, plasminogen, which can be converted to plasmin by plasminogen activator. 18
  • 19. Plasminogen activator Two main types : urokinase (uPA) and tissue (tPA). uPA is bound to the surface of tumor cells by means of a specific receptor (uPAR) There are specific inhibitors (PAI-1 and PAI-2) for the PA. 19
  • 20. Interaction between tumour cells and the surrounding connective tissue 20
  • 21. Cell adhesion and metastasis 21
  • 22. b) Cell attachment 1. Integrin: cell-matrix adhesion 2. E- cadherin/catenin adhesion complex: cell-cell adhesion 22
  • 23. 1) Integrin Heterodimeric transmembrane receptors consists of α and β subunits Function to provide interactions between cells and macromolecules in the ECM Integrin can affect the transcription of MMP genes 23
  • 25. 2) E- cadherin and catenin complex Most important cell-cell adhesion molecules Reduce expression of E-cadherin and catenin increase the invasiveness of tumor cells 25
  • 28. 28
  • 29. c) Cell migration 1. Small Rho GTPase family 2. Motility promoting factors 29
  • 30. Small Rho GTPase Stimuli Cdc42 Rac1 GTP GTP Pak1 MLC Kinase LIM kinase Stress fibers MLC Phosphorylation Cofilin Contraction Filopodia Actin polymerisation Detachment Lamellipodia 30
  • 31. Model of Rho GTPase regulation 31
  • 32. Regulation of Rho GTPase 32
  • 33. Rho GTPase is required for the transition of invasive phenotype 33
  • 34. Signaling pathways related to integrin and small GTPase 34
  • 35. E-cadherin and Rho GTPase signaling 35
  • 36. Rho GTPase at different stages of tumour progression 36
  • 37. 2) Motility promoting factors Hepatocyte growth factor/scattering factor Insulin-like growth factor II Autotaxin 37
  • 38. HGF/scatting factor Heterodimer of α and β chains HGF normally acts as a paracrine growth factor, but in tumor cells it can act as an autocrine HGF binds to the c-Met receptor and activated the downstream effectors 38
  • 39. HGF induce cell scattering and invasion 39
  • 40. Signalling pathways responsible for MET-dependent invasive growth 40